[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 11536
1. Usui S, Oveson BC, Lee SY, Jo YJ, Yoshida T, Miki A, Miki K, Iwase T, Lu L, Campochiaro PA: NADPH oxidase plays a central role in cone cell death in retinitis pigmentosa. J Neurochem; 2009 Aug;110(3):1028-37
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • After rods die, the level of tissue oxygen in the outer retina becomes elevated and there is progressive oxidative damage to cones that ultimately triggers apoptosis.
  • Apocynin, a blocker of Nox, but not allopurinol, a blocker of xanthine oxidase, markedly reduced the superoxide radicals visualized by hydroethidine in the outer retina in the retinal degeneration-1 (rd1(+/+)) model of RP.
  • Compared to rd1(+/+) mice treated with vehicle, those treated with apocynin, but not those treated with allopurinol, had significantly less oxidative damage in the retina measured by ELISA for carbonyl adducts.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 1990 Jan 25;343(6256):364-6 [2137202.001]
  • [Cites] Antioxid Redox Signal. 2009 Apr;11(4):715-24 [18823256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Apr 15;89(8):3362-6 [1314387.001]
  • [Cites] Brain Res. 1992 Aug 14;588(1):21-8 [1393569.001]
  • [Cites] Nat Genet. 1993 Jun;4(2):130-4 [8394174.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1994 Oct;35(11):3897-904 [7928187.001]
  • [Cites] J Neurosci. 1994 Oct;14(10):5818-33 [7523628.001]
  • [Cites] J Biol Chem. 1995 Apr 7;270(14):7853-7 [7713877.001]
  • [Cites] FASEB J. 1995 Aug;9(11):995-1003 [7649415.001]
  • [Cites] Arch Biochem Biophys. 1998 May 15;353(2):312-21 [9606965.001]
  • [Cites] J Cell Physiol. 1999 May;179(2):149-56 [10199554.001]
  • [Cites] J Biol Chem. 1999 May 28;274(22):15493-9 [10336441.001]
  • [Cites] Lab Invest. 1999 Aug;79(8):967-74 [10462034.001]
  • [Cites] Prog Retin Eye Res. 1999 Nov;18(6):689-735 [10530749.001]
  • [Cites] J Cell Physiol. 2005 Jun;203(3):457-64 [15744744.001]
  • [Cites] Neuroscience. 2005;132(2):233-8 [15802177.001]
  • [Cites] Am J Pathol. 2005 Aug;167(2):599-607 [16049343.001]
  • [Cites] Vis Neurosci. 2005 Jul-Aug;22(4):501-7 [16212707.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jul 25;103(30):11300-5 [16849425.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Aug;47(8):3683-9 [16877443.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 8;103(32):12132-7 [16877542.001]
  • [Cites] Arch Ophthalmol. 2007 Feb;125(2):151-8 [17296890.001]
  • [Cites] Free Radic Biol Med. 2007 Aug 1;43(3):319-31 [17602947.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Nov;41(12):3999-4006 [11053305.001]
  • [Cites] J Cereb Blood Flow Metab. 2001 Apr;21(4):374-84 [11323523.001]
  • [Cites] Am J Cardiol. 2001 Jul 15;88(2):188-91, A6 [11448423.001]
  • [Cites] Am J Pathol. 2001 Sep;159(3):1113-20 [11549604.001]
  • [Cites] Circulation. 2001 Nov 13;104(20):2407-11 [11705816.001]
  • [Cites] Arch Biochem Biophys. 2002 Jan 15;397(2):342-4 [11795892.001]
  • [Cites] Neuron. 2002 Aug 1;35(3):419-32 [12165466.001]
  • [Cites] Exp Eye Res. 2003 Apr;76(4):463-71 [12634111.001]
  • [Cites] J Neurosci. 2003 May 15;23(10):4164-72 [12764104.001]
  • [Cites] Dev Ophthalmol. 2003;37:126-40 [12876834.001]
  • [Cites] J Physiol. 2003 Oct 15;552(Pt 2):335-44 [14561818.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Jun;45(6):2013-9 [15161870.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1978 Jun;17(6):489-98 [659071.001]
  • [Cites] J Biol Chem. 1981 Sep 10;256(17):9090-5 [6894924.001]
  • [Cites] Cell. 1981 Jul;25(1):67-82 [6895049.001]
  • [Cites] Arch Biochem Biophys. 1982 Sep;217(2):401-10 [6291460.001]
  • [Cites] Differentiation. 1983;23(3):218-25 [6687872.001]
  • [Cites] J Mol Cell Cardiol. 1985 Feb;17(2):145-52 [3839024.001]
  • [Cites] J Clin Invest. 1988 Apr;81(4):1297-301 [3127425.001]
  • [Cites] J Appl Physiol (1985). 1988 Nov;65(5):2349-53 [3209579.001]
  • [Cites] Mol Vis. 2007;13:840-53 [17615545.001]
  • [Cites] J Cell Physiol. 2007 Dec;213(3):809-15 [17520694.001]
  • [Cites] Science. 2007 Dec 7;318(5856):1645-7 [18063801.001]
  • [Cites] J Cell Physiol. 2008 Oct;217(1):13-22 [18543272.001]
  • [Cites] Mol Ther. 2008 Oct;16(10):1688-94 [18665154.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 Oct;49(10):4561-7 [18539939.001]
  • [Cites] Free Radic Biol Med. 2008 Sep 15;45(6):905-12 [18634866.001]
  • [Cites] Mol Neurobiol. 2008 Dec;38(3):253-69 [18982459.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Aug 1;88(15):6481-5 [1862076.001]
  • (PMID = 19493169.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY005951-23; United States / NEI NIH HHS / EY / R01 EY005951; United States / NEI NIH HHS / EY / R01 EY005951-23; United States / NEI NIH HHS / EY / R01 EY05951
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 1.6.3.1 / NADPH Oxidase
  • [Other-IDs] NLM/ NIHMS170296; NLM/ PMC2833098
  •  go-up   go-down


2. Hegde GV, James J, Das AV, Zhao X, Bhattacharya S, Ahmad I: Characterization of early retinal progenitor microenvironment: presence of activities selective for the differentiation of retinal ganglion cells and maintenance of progenitors. Exp Eye Res; 2007 Mar;84(3):577-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of early retinal progenitor microenvironment: presence of activities selective for the differentiation of retinal ganglion cells and maintenance of progenitors.
  • The maintenance and differentiation of retinal progenitors take place in the context of the microenvironment in which they reside at a given time during retinal histogenesis.
  • To understand the nature of the microenvironment in the developing retina, we have examined the influence of activities present during the early stage of retinal histogenesis on enriched retinal progenitors, using the neurosphere model.
  • Early and late retinal progenitors, enriched as neurospheres from embryonic day 14 (E14) and E18 rat retina, respectively, were cultured in embryonic day 3 (E3) chick retinal conditioned medium, simulating the microenvironment present during early retinal histogenesis.
  • Examination of the differentiation and proliferation of retinal progenitors revealed that the early microenvironment contains at least three regulatory activities, which are partitioned in different size fractions of the conditioned medium with different heat sensitivity.
  • First, it is characterized by activities, present in heat stable <30 kDa fraction, that promote the differentiation of retinal ganglion cells (RGCs), the early born neurons.
  • Second, it contains activities, present in heat-sensitive >30 kDa fraction, that regulate the number of early born neurons and maintain the pool of retinal progenitors.
  • Third, it possesses activities, present in heat-sensitive <30 kDa fraction, that prevent the premature differentiation of early retinal progenitors into the late born neurons.
  • Thus, our observations demonstrate the regulatory influence of microenvironment on the maintenance and differentiation of retinal progenitors and establish neurospheres as a viable model system for the examination of such influences.
  • [MeSH-major] Retina / embryology. Stem Cells / cytology
  • [MeSH-minor] Animals. Cell Differentiation. Cell Division. Cells, Cultured. Coculture Techniques. Culture Media, Conditioned. Female. Gene Expression Regulation, Developmental. Immunohistochemistry / methods. Models, Animal. Photoreceptor Cells, Vertebrate / cytology. Rats. Rats, Sprague-Dawley. Retinal Ganglion Cells / cytology. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17227675.001).
  • [ISSN] 0014-4835
  • [Journal-full-title] Experimental eye research
  • [ISO-abbreviation] Exp. Eye Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media, Conditioned
  •  go-up   go-down


3. Liao SD, Puro DG: NAD+-induced vasotoxicity in the pericyte-containing microvasculature of the rat retina: effect of diabetes. Invest Ophthalmol Vis Sci; 2006 Nov;47(11):5032-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NAD+-induced vasotoxicity in the pericyte-containing microvasculature of the rat retina: effect of diabetes.
  • PURPOSE: It was recently proposed that activation of P2X(7) purinoceptors may play a role in causing cell death in the pericyte-containing microvasculature of the diabetic retina.
  • This hypothesis is supported by the observation that diabetes enhances lethal pore formation in retinal microvessels exposed to synthetic P2X(7) agonists.
  • METHODS: Pericyte-containing retinal microvessels were isolated from normal and streptozotocin-injected rats.
  • RESULTS: In freshly isolated retinal microvessels, it was found that extracellular NAD(+), but not its catabolites, caused cell death (half-maximal effective concentration [EC(50)] = 2 nM) by a mechanism involving the activation of P2X(7) purinoceptors and the formation of transmembrane pores.
  • A series of experiments provided evidence that NAD(+), which is not a direct purinergic agonist, serves as a substrate for ecto-ribosylation reactions that subsequently trigger P2X(7)-dependent cell death in the retinal microvasculature.
  • Soon after the onset of diabetes, the sensitivity of retinal microvessels to the vasotoxic effect of extracellular NAD(+) increased by approximately 100-fold.
  • CONCLUSIONS: Purinergic vasotoxicity triggered by extracellular NAD(+) is a newly recognized mechanism that may contribute to the cell death observed in the pericyte-containing microvascular of the diabetic retina.
  • [MeSH-major] Apoptosis / drug effects. Diabetes Mellitus, Experimental / metabolism. Diabetic Retinopathy / metabolism. NAD / toxicity. Pericytes / drug effects. Retinal Vessels / drug effects

  • MedlinePlus Health Information. consumer health - Diabetic Eye Problems.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17065524.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY 07003; United States / NEI NIH HHS / EY / EY 12505
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzoxazoles; 0 / Fluorescent Dyes; 0 / P2rx7 protein, rat; 0 / Purinergic P2 Receptor Antagonists; 0 / Quinolinium Compounds; 0 / Receptors, Purinergic P2; 0 / Receptors, Purinergic P2X7; 0U46U6E8UK / NAD; 152068-09-2 / YO-PRO 1; 20762-30-5 / Adenosine Diphosphate Ribose; 38806-39-2 / 1,N(6)-ethenoadenosine diphosphate; 61D2G4IYVH / Adenosine Diphosphate; EC 2.4.2.- / ADP Ribose Transferases
  •  go-up   go-down


Advertisement
4. Cheruvu NP, Amrite AC, Kompella UB: Effect of eye pigmentation on transscleral drug delivery. Invest Ophthalmol Vis Sci; 2008 Jan;49(1):333-41
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: To determine the influence of eye pigmentation on transscleral retinal delivery of celecoxib.
  • The animals were euthanatized at the end of 0.25, 0.5, 1, 2, 3, 4, 8, or 12 hours after the drug was administered, and celecoxib levels in ocular tissues (sclera, choroid-RPE, retina, vitreous, lens, and cornea) were estimated with an HPLC assay.
  • RESULTS: The r(max) and k for celecoxib's binding to natural melanin were (3.92 +/- 0.06) x 10(-7) moles/mg of melanin and (0.08 +/- 0.01) x 10(6) M(-1), respectively.
  • The concentrations of melanin in choroid-RPE, sclera, and retina of BN rats were 200 +/- 30, 12 +/- 4, and 3 +/- 0.2 mug/mg tissue, respectively.
  • However, the retinal (P = 0.001) and vitreal (P = 0.001) AUCs of celecoxib in the treated eyes were approximately 1.5-fold higher in SD rats than in BN rats.
  • With celecoxib-poly(lactide) microparticles, choroid-RPE, retina, and vitreous concentrations on day 8 exhibited similar trends in differences between the two strains, with the differences being greater than those recorded for the celecoxib suspension.
  • CONCLUSIONS: Transscleral retinal and vitreal drug delivery of lipophilic celecoxib is significantly lower in pigmented rats than in albino rats.
  • The hindrance of retinal and vitreal drug delivery by the choroid-RPE in pigmented rats is also true of sustained-release microparticle systems.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CELECOXIB .
  • Hazardous Substances Data Bank. LACTIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Apr;41(5):1181-5 [10752958.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Mar;47(3):1149-60 [16505053.001]
  • [Cites] Adv Drug Deliv Rev. 2001 Oct 31;52(1):37-48 [11672874.001]
  • [Cites] Drug Metab Dispos. 2002 Apr;30(4):421-9 [11901096.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Apr;43(4):1198-203 [11923266.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Jun;43(6):1809-16 [12036983.001]
  • [Cites] Prog Retin Eye Res. 2002 Mar;21(2):145-51 [12062532.001]
  • [Cites] Surv Ophthalmol. 2002 Aug;47 Suppl 1:S41-52 [12204700.001]
  • [Cites] J Ocul Pharmacol Ther. 2002 Aug;18(4):325-37 [12222763.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Mar;44(3):1192-201 [12601049.001]
  • [Cites] J Pharm Pharmacol. 2003 Aug;55(8):1127-33 [12956903.001]
  • [Cites] J Pharm Pharmacol. 2003 Dec;55(12):1647-54 [14738591.001]
  • [Cites] Arch Ophthalmol. 1974 Oct;92(4):315-7 [4412575.001]
  • [Cites] Am J Ophthalmol. 1977 Mar;83(3):407-13 [848547.001]
  • [Cites] Ophthalmic Res. 1988;20(1):31-43 [3380524.001]
  • [Cites] Exp Eye Res. 1988 Oct;47(4):565-77 [2903066.001]
  • [Cites] J Ocul Pharmacol. 1992 Spring;8(1):35-42 [1402293.001]
  • [Cites] Cornea. 1992 Jul;11(4):329-33 [1424654.001]
  • [Cites] Ophthalmology. 1993 Mar;100(3):373-6 [8460008.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Oct;47(10):4513-22 [17003447.001]
  • [Cites] Pigment Cell Res. 2006 Dec;19(6):572-94 [17083485.001]
  • [Cites] J Drug Target. 2006 Dec;14(10):670-9 [17162736.001]
  • [Cites] Expert Opin Drug Deliv. 2007 Jan;4(1):77-85 [17184164.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Apr;41(5):1186-91 [10752959.001]
  • [Cites] J Ocul Pharmacol. 1994 Spring;10(1):217-39 [8207328.001]
  • [Cites] Antimicrob Agents Chemother. 1995 Apr;39(4):834-8 [7785980.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1996 Mar;37(4):613-8 [8595961.001]
  • [Cites] Br J Ophthalmol. 1996 Aug;80(8):685-8 [8949709.001]
  • [Cites] Eur J Pharm Biopharm. 1998 Jul;46(1):39-50 [9700021.001]
  • [Cites] Regul Toxicol Pharmacol. 1998 Oct;28(2):124-32 [9927562.001]
  • [Cites] Am J Ophthalmol. 1999 Aug;128(2):192-7 [10458175.001]
  • [Cites] Biol Pharm Bull. 1999 Sep;22(9):956-60 [10513620.001]
  • [Cites] Biol Pharm Bull. 1999 Sep;22(9):961-5 [10513621.001]
  • [Cites] Am J Ophthalmol. 1964 Sep;58:362-6 [14204798.001]
  • [Cites] Lancet. 1959 Oct 3;2(7101):478-80 [14402143.001]
  • [Cites] Pharm Res. 2004 Oct;21(10):1797-804 [15553225.001]
  • [Cites] Eur J Pharmacol. 2005 Mar 28;511(2-3):191-8 [15792788.001]
  • [Cites] Ophthalmology. 2005 Jun;112(6):1151-8 [15885791.001]
  • [Cites] Expert Opin Drug Deliv. 2004 Nov;1(1):99-114 [16296723.001]
  • [Cites] Pigment Cell Res. 2000 Jun;13(3):179-84 [10885677.001]
  • (PMID = 18172110.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK064172; United States / NEI NIH HHS / EY / R24 EY017045-02; United States / NIDDK NIH HHS / DK / R01 DK064172-02S1; United States / NIDDK NIH HHS / DK / DK 064172; United States / NIDDK NIH HHS / DK / R01 DK064172-03; United States / NEI NIH HHS / EY / R24 EY017045; United States / NEI NIH HHS / EY / EY 017045; United States / NEI NIH HHS / EY / R03 EY013842; United States / NEI NIH HHS / EY / EY 013842
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Drug Carriers; 0 / Melanins; 0 / Polymers; 0 / Pyrazoles; 0 / Sulfonamides; 0 / polylactic acid-polyglycolic acid copolymer; 26009-03-0 / Polyglycolic Acid; 33X04XA5AT / Lactic Acid; JCX84Q7J1L / Celecoxib
  • [Other-IDs] NLM/ NIHMS367015; NLM/ PMC3324932
  •  go-up   go-down


5. Mora-Ferrer C, Neumeyer C: Neuropharmacology of vision in goldfish: a review. Vision Res; 2009 May;49(9):960-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The goldfish is one of the few animals exceptionally well analyzed in behavioral experiments and also in electrophysiological and neuroanatomical investigations of the retina.
  • To get insight into the functional organization of the retina we studied color vision, motion detection and temporal resolution before and after intra-ocular injection of neuropharmaca with known effects on retinal neurons.
  • [MeSH-major] Goldfish / physiology. Neurotransmitter Agents / pharmacology. Retina / physiology. Vision, Ocular / physiology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOPAMINE .
  • Hazardous Substances Data Bank. GLYCINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18768148.001).
  • [ISSN] 1878-5646
  • [Journal-full-title] Vision research
  • [ISO-abbreviation] Vision Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neurotransmitter Agents; 56-12-2 / gamma-Aminobutyric Acid; N9YNS0M02X / Acetylcholine; TE7660XO1C / Glycine; VTD58H1Z2X / Dopamine
  •  go-up   go-down


6. Kamphuis W, Dijk F, Bergen AA: Ischemic preconditioning alters the pattern of gene expression changes in response to full retinal ischemia. Mol Vis; 2007;13:1892-901
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ischemic preconditioning alters the pattern of gene expression changes in response to full retinal ischemia.
  • PURPOSE: Ischemic conditions in the retina have been implicated in several retinopathological conditions.
  • Experimentally induced ischemia for 60 min followed by reperfusion leads to a loss of neurons in the inner retina.
  • In contrast, a 5 min ischemic episode triggers a series of alterations that protect the retina against the damaging effects of a subsequent 60 min ischemic insult.
  • To study the changes altered by IPC, we assessed the gene expression patterns in the rat retina after ischemia (60 min) followed by reperfusion (I/R) and compared these to the gene expression patterns after ischemia/reperfusion in preconditioned animals (IPC-I/R).
  • Our observations indicate that activation of translational activity may be a mediator of ischemia-associated damage in the retina, and IPC may prevent activation of this mechanism.
  • [MeSH-major] Gene Expression Regulation. Ischemia / metabolism. Ischemic Preconditioning. Retinal Vessels

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17960128.001).
  • [ISSN] 1090-0535
  • [Journal-full-title] Molecular vision
  • [ISO-abbreviation] Mol. Vis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9014-25-9 / RNA, Transfer; EC 6.1.1.- / Amino Acyl-tRNA Synthetases
  •  go-up   go-down


7. Albanna W, Banat M, Albanna N, Alnawaiseh M, Siapich SA, Igelmund P, Weiergräber M, Lüke M, Schneider T: Longer lasting electroretinographic recordings from the isolated and superfused murine retina. Graefes Arch Clin Exp Ophthalmol; 2009 Oct;247(10):1339-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Longer lasting electroretinographic recordings from the isolated and superfused murine retina.
  • BACKGROUND: Analysis of retinal signaling in mutant mice has become a powerful tool for studying retinal function and disease.
  • Previous attempts to record from isolated mouse retina have been limited to short time periods (about 90 min).
  • We performed a series of recordings from isolated mouse retina under a number of different conditions in order to determine the optimal parameters for this species.
  • METHODS: We used a superfused vertebrate retina assay, for which the murine retina had to be isolated with specific tools.
  • RESULTS: To improve the sensitivity and stability of photoreceptor and retinal network responses from the isolated and superfused murine retina, two different nutrient solutions from rat (physiological Ca(2+)) and bovine (reduced Ca(2+) but increased phosphate buffering capacity) were used.
  • Further, a temperature reduced to 27.5 degrees C, a light intensity ten-fold increased (63 mlux), and an increased flow rate (2 ml/min) provided conditions under which the b-wave response was stable for more than 3 hours.
  • CONCLUSION: In conclusion, the isolated murine retina can be used as a pharmacological testing system, which provides the additional advantage of selective gene inactivation for better understanding of retinal signalling.
  • [MeSH-major] Electroretinography. Mice. Retina / physiology

  • Hazardous Substances Data Bank. NICKEL, ELEMENTAL .
  • Hazardous Substances Data Bank. NICKEL CHLORIDE .
  • Hazardous Substances Data Bank. OXYGEN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Invest Ophthalmol Vis Sci. 1997 Apr;38(5):792-9 [9112973.001]
  • [Cites] Genes Brain Behav. 2006 Jul;5(5):389-403 [16879633.001]
  • [Cites] Vision Res. 2000;40(13):1653-65 [10814754.001]
  • [Cites] Vis Neurosci. 1995 Sep-Oct;12(5):837-50 [8924408.001]
  • [Cites] Vision Res. 1999 Jun;39(13):2165-77 [10343799.001]
  • [Cites] Neurobiol Aging. 2007 Oct;28(10):1577-93 [17010477.001]
  • [Cites] Vis Neurosci. 2004 Sep-Oct;21(5):739-47 [15683561.001]
  • [Cites] Doc Ophthalmol. 2003 Jul;107(1):13-36 [12906119.001]
  • [Cites] Front Biosci. 2008 May 01;13:6269-75 [18508659.001]
  • [Cites] Acta Ophthalmol. 2008 Sep;86(6):676-82 [18752519.001]
  • [Cites] Mol Endocrinol. 2002 Apr;16(4):884-95 [11923483.001]
  • [Cites] Prog Retin Eye Res. 2005 Nov;24(6):682-720 [16027025.001]
  • [Cites] J Ocul Pharmacol Ther. 2005 Aug;21(4):305-14 [16117694.001]
  • [Cites] Adv Exp Med Biol. 2002;514:465-76 [12596939.001]
  • [Cites] J Neurophysiol. 1963 Jul;26:617-34 [14012566.001]
  • [Cites] Nat Genet. 1998 Jul;19(3):264-7 [9662400.001]
  • [Cites] Science. 1965 Apr 30;148(3670):648-51 [14268730.001]
  • [Cites] J Neurophysiol. 1999 Jun;81(6):2923-36 [10368409.001]
  • [Cites] J Neurosci. 1992 Mar;12(3):840-53 [1312136.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 1994 May;232(5):318-23 [8045442.001]
  • [Cites] Vis Neurosci. 1999 May-Jun;16(3):503-11 [10349971.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Jun;44(6):2708-15 [12766077.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1987 Jan;28(1):34-49 [3026986.001]
  • [Cites] Brain Res Brain Res Protoc. 2005 Dec;16(1-3):27-36 [16275053.001]
  • [Cites] Vis Neurosci. 1998 May-Jun;15(3):541-52 [9685206.001]
  • [Cites] Acta Ophthalmol. 2009 Nov;87(8):854-65 [20002018.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 2005 Sep;243(9):933-41 [15838665.001]
  • [Cites] Neuron. 2001 Oct 11;32(1):89-98 [11604141.001]
  • [Cites] J Neurosci. 2004 Feb 18;24(7):1707-18 [14973233.001]
  • [Cites] Clin Neurosci. 1997;4(6):327-35 [9358976.001]
  • [Cites] Annu Rev Neurosci. 2001;24:779-805 [11520918.001]
  • [Cites] Clin Neurosci. 1997;4(6):336-40 [9358977.001]
  • [Cites] J Med Genet. 2006 Aug;43(8):699-704 [16505158.001]
  • [Cites] Vis Neurosci. 2004 Mar-Apr;21(2):129-34 [15259564.001]
  • [Cites] Mamm Genome. 2000 Jul;11(7):531-6 [10886018.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1990 Oct;31(10):2070-81 [2211004.001]
  • [Cites] Vis Neurosci. 1992 Feb;8(2):107-26 [1558823.001]
  • [Cites] Adv Exp Med Biol. 1972;24(0):101-18 [4546796.001]
  • [Cites] J Physiol. 1933 Feb 8;77(3):207-39 [16994385.001]
  • [Cites] Nat Genet. 1998 Jul;19(3):260-3 [9662399.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2007 Jun;48(6):2498-502 [17525176.001]
  • (PMID = 19629513.001).
  • [ISSN] 1435-702X
  • [Journal-full-title] Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie
  • [ISO-abbreviation] Graefes Arch. Clin. Exp. Ophthalmol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Solutions; 696BNE976J / nickel chloride; 7OV03QG267 / Nickel; S88TT14065 / Oxygen; YO1UK1S598 / Isradipine
  •  go-up   go-down


8. Sanders EJ, Lin WY, Parker E, Harvey S: Growth hormone expression and neuroprotective activity in a quail neural retina cell line. Gen Comp Endocrinol; 2010 Jan 1;165(1):111-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth hormone expression and neuroprotective activity in a quail neural retina cell line.
  • We have previously shown that growth hormone (GH) is produced within cells of the chick embryo retina where it appears to act as an autocrine/paracrine anti-apoptotic factor in the regulation of programmed cell death during retinal development.
  • These investigations were carried out on cultured chick embryo retinal ganglion cells (RGCs) as well as on the chick embryo retina in ovo, using GH protein knock-down by immunoneutralization.
  • We have now investigated the putative neuroprotective actions of GH using a quail embryo neural retina cell line (QNR/D) treated with GH siRNA to silence the local synthesis of GH.
  • We now show that knock-down of GH by gene silencing in cells of this cultured embryonic neural retina cell line, using NR-cGH-1 siRNA, correlates with the increased appearance in the cultures of cells with apoptotic nuclear morphology.
  • We thus validate, using different technology and a different culture system, our contention that GH, produced locally by cells of the neural retina acts in an autocrine or paracrine manner to regulate cell survival in the retina.
  • [MeSH-major] Gene Expression Regulation. Growth Hormone / metabolism. Retina / cytology. Retina / metabolism. Retinal Ganglion Cells / metabolism

  • COS Scholar Universe. author profiles.
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19539627.001).
  • [ISSN] 1095-6840
  • [Journal-full-title] General and comparative endocrinology
  • [ISO-abbreviation] Gen. Comp. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Small Interfering; 9002-72-6 / Growth Hormone
  •  go-up   go-down


9. See AW, Clagett-Dame M: The temporal requirement for vitamin A in the developing eye: mechanism of action in optic fissure closure and new roles for the vitamin in regulating cell proliferation and adhesion in the embryonic retina. Dev Biol; 2009 Jan 1;325(1):94-105
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The temporal requirement for vitamin A in the developing eye: mechanism of action in optic fissure closure and new roles for the vitamin in regulating cell proliferation and adhesion in the embryonic retina.
  • The optic fissure does not close in late VAD embryos, and severe folding and collapse of the retina is observed at E18.5.
  • Surprisingly, ROL given as late as E13.5 completely prevents folding of the retina despite the presence of an open fetal fissure, showing that coloboma and retinal folding represent distinct VAD-dependent defects.
  • Retinal folding due to VAD is preceded by an overall reduction in the percentage of cyclin D1 positive cells in the developing retina, (initially resulting in retinal thinning), as well as a dramatic reduction in the cell adhesion-related molecules, N-cadherin and beta-catenin.
  • Reduction of retinal cell number combined with a loss of the normal cell-cell adhesion proteins may contribute to the collapse and folding of the retina that occurs in late VAD fetuses.
  • [MeSH-major] Retina / cytology. Retina / embryology. Vitamin A / metabolism
  • [MeSH-minor] Animals. Basement Membrane / drug effects. Basement Membrane / pathology. Cadherins / metabolism. Cell Adhesion / drug effects. Cell Death / drug effects. Cell Differentiation / drug effects. Cell Proliferation / drug effects. Coloboma / complications. Coloboma / embryology. Coloboma / genetics. Cyclin D1 / metabolism. Down-Regulation / drug effects. Embryo, Mammalian / abnormalities. Embryo, Mammalian / drug effects. Fetus / abnormalities. Fetus / drug effects. Gene Expression Regulation, Developmental / drug effects. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Retinal Ganglion Cells / cytology. Retinal Ganglion Cells / drug effects. Time Factors. Transcription Factors / genetics. Transcription Factors / metabolism. Vitamin A Deficiency / embryology. Vitamin A Deficiency / genetics. beta Catenin / metabolism


10. Gunnersen JM, Kuek A, Phipps JA, Hammond VE, Puthussery T, Fletcher EL, Tan SS: Seizure-related gene 6 (Sez-6) in amacrine cells of the rodent retina and the consequence of gene deletion. PLoS One; 2009;4(8):e6546
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Seizure-related gene 6 (Sez-6) in amacrine cells of the rodent retina and the consequence of gene deletion.
  • BACKGROUND: Seizure-related gene 6 (Sez-6) is expressed in neurons of the mouse brain, retina and spinal cord.
  • METHODOLOGY/PRINCIPAL FINDINGS: The distribution pattern of Sez-6 in the retina was studied using a polyclonal antibody that detects the multiple isoforms of Sez-6.
  • Prominent immunostaining was detected in GABAergic, but not in AII glycinergic, amacrine cell subpopulations of the rat and mouse retina.
  • In order to assess the role of Sez-6 in the retina, we analyzed the morphology of the Sez-6 knockout mouse retina with immunohistochemical markers and compared ganglion cell dendritic arbor patterning in Sez-6 null retinae with controls.
  • CONCLUSIONS: In summary, we have reported the detailed expression pattern of a novel retinal marker with broad cell specificity, useful for retinal characterization in rodent experimental models.
  • Retinal morphology, ganglion cell dendritic branching and ERG waveforms appeared normal in the Sez-6 knockout mouse suggesting that, in spite of widespread expression of Sez-6, retinal function in the absence of Sez-6 is not affected.
  • [MeSH-major] Amacrine Cells / metabolism. Gene Deletion. Nerve Tissue Proteins / genetics. Retina / metabolism


11. Livne-Bar I, Pacal M, Cheung MC, Hankin M, Trogadis J, Chen D, Dorval KM, Bremner R: Chx10 is required to block photoreceptor differentiation but is dispensable for progenitor proliferation in the postnatal retina. Proc Natl Acad Sci U S A; 2006 Mar 28;103(13):4988-93
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chx10 is required to block photoreceptor differentiation but is dispensable for progenitor proliferation in the postnatal retina.
  • In the Chx10-null ocular retardation (or(J)) mouse, retinal progenitor cell (RPC) proliferation is impaired, and bipolar neurons, a late born cell type, fail to differentiate.
  • In the Chx10 null or(J) retina, only a small fraction of cells expressing mutated Chx10 mRNA were rods, but this fraction increased after p27(Kip1) inactivation, which partially rescues proliferation.
  • Most significantly, acute Chx10 knockdown in the postnatal retina promoted rods in place of bipolar neurons without affecting division.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurobiol. 2000 Feb 5;42(2):232-47 [10640330.001]
  • [Cites] J Biol Chem. 2006 Jan 13;281(2):744-51 [16236706.001]
  • [Cites] Development. 2001 Apr;128(8):1313-22 [11262232.001]
  • [Cites] J Biol Chem. 2001 Feb 9;276(6):4109-18 [11069920.001]
  • [Cites] Hum Mol Genet. 2001 Jul 15;10(15):1571-9 [11468275.001]
  • [Cites] Micron. 2002;33(1):1-6 [11473808.001]
  • [Cites] Nat Genet. 2001 Dec;29(4):447-52 [11694879.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Nov;43(11):3522-9 [12407164.001]
  • [Cites] Development. 2003 Feb;130(3):539-52 [12490560.001]
  • [Cites] Development. 2003 Apr;130(7):1281-94 [12588845.001]
  • [Cites] Glia. 2003 Jul;43(1):70-6 [12761869.001]
  • [Cites] Nat Neurosci. 2003 Dec;6(12):1255-63 [14625556.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jan 6;101(1):16-22 [14603031.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Feb;45(2):375-84 [14744875.001]
  • [Cites] Semin Cell Dev Biol. 2004 Feb;15(1):83-9 [15036211.001]
  • [Cites] Dev Biol. 2004 Jul 15;271(2):388-402 [15223342.001]
  • [Cites] PLoS Biol. 2004 Sep;2(9):E247 [15226823.001]
  • [Cites] Development. 2004 Oct;131(20):5139-52 [15459106.001]
  • [Cites] Anat Rec. 1985 Jun;212(2):199-205 [3842042.001]
  • [Cites] Nature. 1987 Jul 9-15;328(6126):131-6 [3600789.001]
  • [Cites] Genes Dev. 1993 Nov;7(11):2120-34 [7901121.001]
  • [Cites] Neuron. 1994 Aug;13(2):377-93 [7914735.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 23;93(2):589-95 [8570600.001]
  • [Cites] Nat Genet. 1996 Apr;12(4):376-84 [8630490.001]
  • [Cites] Mech Dev. 1997 May;63(2):133-43 [9203137.001]
  • [Cites] J Comp Neurol. 1997 Oct 27;387(3):439-48 [9335426.001]
  • [Cites] J Comp Neurol. 1997 Nov 24;388(3):495-505 [9368856.001]
  • [Cites] Methods. 1998 Apr;14(4):393-406 [9608510.001]
  • [Cites] Mech Dev. 1998 Oct;77(2):149-64 [9831642.001]
  • [Cites] Development. 2005 Jan;132(1):177-87 [15576400.001]
  • [Cites] J Biol Chem. 2005 Mar 18;280(11):10100-8 [15647262.001]
  • [Cites] Nucleic Acids Res. 2005;33(8):2661-75 [15886395.001]
  • [Cites] Dev Biol. 2005 Sep 1;285(1):101-15 [16040025.001]
  • [Cites] Brain Res Mol Brain Res. 2000 May 31;78(1-2):26-37 [10891582.001]
  • (PMID = 16547132.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / Vsx2 protein, mouse
  • [Other-IDs] NLM/ PMC1458782
  •  go-up   go-down


12. Lohr HR, Kuntchithapautham K, Sharma AK, Rohrer B: Multiple, parallel cellular suicide mechanisms participate in photoreceptor cell death. Exp Eye Res; 2006 Aug;83(2):380-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In previous experiments, analyzing gene expression in the degenerating rd/rd mouse retina, we have suggested that the gene defect leads to oxidative stress and altered metabolism, which may induce caspase-dependent and caspase-independent cell death mechanisms such as the activation of cystein-proteases, lysosomal proteases, autophagy and complement-mediated lysis.
  • The presence of the marker genes was verified by laser capture microdissection, and apoptosis (caspase activity) and autophagy (lysozyme and cathepsin activity) were verified in retina extracts.
  • The temporal pattern of the different pathways suggests that the non-caspase-dependent mechanisms may actively participate in the demise of the photoreceptors, rather than represent a passive response of the retina to the presence of dying cells.
  • [MeSH-major] Cell Death / physiology. Photoreceptor Cells, Vertebrate / physiology. Retinal Degeneration / physiopathology

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Autophagy. 2007 Jan-Feb;3(1):65-6 [17102584.001]
  • [ErratumIn] Exp Eye Res. 2006 Dec;83(6):1522
  • (PMID = 16626700.001).
  • [ISSN] 0014-4835
  • [Journal-full-title] Experimental eye research
  • [ISO-abbreviation] Exp. Eye Res.
  • [Language] eng
  • [Grant] United States / NIDCR NIH HHS / DE / DE-FG02-01ER63121; United States / NEI NIH HHS / EY / EY-13520; United States / NEI NIH HHS / EY / EY-14793
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers; EC 3.2.1.17 / Muramidase; EC 3.4.22.36 / Caspase 1
  •  go-up   go-down


13. Noma H, Funatsu H, Mimura T, Hori S: Changes of vascular endothelial growth factor after vitrectomy for macular edema secondary to retinal vein occlusion. Eur J Ophthalmol; 2008 Nov-Dec;18(6):1017-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Changes of vascular endothelial growth factor after vitrectomy for macular edema secondary to retinal vein occlusion.
  • PURPOSE: To examine whether vitrectomy combined with retinal photocoagulation reduces the vitreous level of vascular endothelial growth factor (VEGF) in patients with macular edema associated with retinal vein occlusion (RVO).
  • During vitrectomy, retinal photocoagulation was performed on the ischemic region of the retina in all cases (mean of 510 shots).
  • CONCLUSIONS: The results suggest that the vitreous levels of VEGF may be reduced by vitrectomy combined with retinal photocoagulation for macular edema with RVO.
  • It may be important to reduce the vitreous levels of VEGF by vitrectomy and retinal photocoagulation for ischemic retina in macular edema with RVO.
  • [MeSH-major] Macular Edema / metabolism. Macular Edema / surgery. Retinal Vein Occlusion / metabolism. Vascular Endothelial Growth Factor A / metabolism. Vitrectomy. Vitreous Body / metabolism

  • Genetic Alliance. consumer health - Edema.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18988180.001).
  • [ISSN] 1120-6721
  • [Journal-full-title] European journal of ophthalmology
  • [ISO-abbreviation] Eur J Ophthalmol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
  •  go-up   go-down


14. Wielgus AR, Chignell CF, Miller DS, Van Houten B, Meyer J, Hu DN, Roberts JE: Phototoxicity in human retinal pigment epithelial cells promoted by hypericin, a component of St. John's wort. Photochem Photobiol; 2007 May-Jun;83(3):706-13
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phototoxicity in human retinal pigment epithelial cells promoted by hypericin, a component of St. John's wort.
  • To determine if hypericin might also be phototoxic to the human retina, we exposed human retinal pigment epithelial (hRPE) cells to 10(-7) to 10(-5) M hypericin.
  • Thus, ingested SJW is potentially phototoxic to the retina and could contribute to retinal or early macular degeneration.

  • Hazardous Substances Data Bank. PERYLENE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Biochem. 2000 Nov;33(8):619-25 [11166008.001]
  • [Cites] IUBMB Life. 2000 Oct-Nov;50(4-5):315-21 [11327326.001]
  • [Cites] Int Clin Psychopharmacol. 2001 Sep;16(5):239-52 [11552767.001]
  • [Cites] Int J Toxicol. 2001;20 Suppl 2:31-9 [11558639.001]
  • [Cites] J Biol Chem. 2001 Nov 23;276(47):43836-41 [11571295.001]
  • [Cites] J Cosmet Laser Ther. 2001 Sep;3(3):159-60 [12006194.001]
  • [Cites] Methods Mol Biol. 2002;197:159-76 [12013794.001]
  • [Cites] Eur J Pharmacol. 2002 Aug 9;449(3):213-20 [12167462.001]
  • [Cites] J Biol Chem. 2003 Mar 7;278(10):8058-64 [12502708.001]
  • [Cites] Int J Toxicol. 2002 Nov-Dec;21(6):465-72 [12537643.001]
  • [Cites] Int J Toxicol. 2002 Nov-Dec;21(6):491-500 [12537645.001]
  • [Cites] Int J Toxicol. 2002 Nov-Dec;21(6):501-9 [12537646.001]
  • [Cites] Photochem Photobiol. 2003 May;77(5):567-71 [12812302.001]
  • [Cites] Photochem Photobiol. 2003 Jul;78(1):88-92 [12929754.001]
  • [Cites] Int J Oncol. 2003 Nov;23(5):1401-5 [14532982.001]
  • [Cites] Eur J Biochem. 2004 Apr;271(7):1339-47 [15030484.001]
  • [Cites] Cancer Lett. 2004 Apr 30;207(2):175-81 [15072826.001]
  • [Cites] Mutat Res. 1989 Sep;214(1):33-40 [2671699.001]
  • [Cites] Free Radic Biol Med. 1990;9(6):515-40 [2079232.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1993 Jun;34(7):2210-9 [8505203.001]
  • [Cites] J Biol Chem. 1996 Apr 26;271(17):9982-6 [8626637.001]
  • [Cites] Photochem Photobiol. 1994 May;59(5):529-33 [8041807.001]
  • [Cites] Ann Intern Med. 1999 Mar 16;130(6):510-4 [10075619.001]
  • [Cites] Curr Med Res Opin. 1999;15(1):33-7 [10216809.001]
  • [Cites] J Pharm Pharmacol. 1999 May;51(5):513-7 [10411209.001]
  • [Cites] Skin Pharmacol Appl Skin Physiol. 1999 Sep-Oct;12(5):299-304 [10461100.001]
  • [Cites] Photochem Photobiol. 2004 Nov-Dec;80(3):583-6 [15623347.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Mar;46(3):1054-61 [15728565.001]
  • [Cites] Prostaglandins Leukot Essent Fatty Acids. 2005 May;72(5):301-25 [15850712.001]
  • [Cites] Int J Oncol. 2005 Jun;26(6):1691-7 [15870887.001]
  • [Cites] Photochem Photobiol. 2005 May-Jun;81(3):524-8 [15643927.001]
  • [Cites] Curr Eye Res. 2000 Aug;21(2):597-601 [11148595.001]
  • [Cites] Methods. 2000 Oct;22(2):135-47 [11020328.001]
  • [Cites] Photochem Photobiol. 2000 Aug;72(2):200-3 [10946573.001]
  • [Cites] Curr Eye Res. 1996 Mar;15(3):255-62 [8654105.001]
  • [Cites] Photochem Photobiol. 1996 Aug;64(2):375-81 [8760577.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):514-9 [9012815.001]
  • [Cites] J Clin Invest. 1998 Mar 15;101(6):1219-24 [9502762.001]
  • [Cites] Free Radic Biol Med. 1998 Mar 15;24(5):699-704 [9586798.001]
  • [Cites] Photochem Photobiol. 1998 Aug;68(2):135-40 [9723207.001]
  • [Cites] FEBS Lett. 1998 Nov 27;440(1-2):19-24 [9862416.001]
  • [Cites] Cancer Res. 1998 Dec 15;58(24):5777-86 [9865736.001]
  • [Cites] BJU Int. 2005 Aug;96(2):217-22 [16001963.001]
  • [Cites] Curr Eye Res. 2005 Apr;30(4):269-77 [16020257.001]
  • [Cites] Eye (Lond). 2006 Feb;20(2):203-7 [15803172.001]
  • (PMID = 17576381.001).
  • [ISSN] 0031-8655
  • [Journal-full-title] Photochemistry and photobiology
  • [ISO-abbreviation] Photochem. Photobiol.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 5QD5427UN7 / Perylene; 7V2F1075HD / hypericin; GAN16C9B8O / Glutathione
  • [Other-IDs] NLM/ NIHMS18993; NLM/ PMC2092452
  •  go-up   go-down


15. Larrosa JM, Polo V, Pérez-Iñigo A, Ferreras A, García-Feijoó J, Antón A, Honrubia FM: [Optic nerve head parameters as measured by confocal scanning laser (Heidelberg Retina Tomograph II) in normal, ocular hypertensive and glaucomatous subjects]. Arch Soc Esp Oftalmol; 2008 Jul;83(7):407-15
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Optic nerve head parameters as measured by confocal scanning laser (Heidelberg Retina Tomograph II) in normal, ocular hypertensive and glaucomatous subjects].
  • [Transliterated title] Estudio de los parámetros de la cabeza del nervio óptico en sujetos normales, hipertensos oculares y glaucomatosos obtenidos mediante láser confocal de barrido (Heidelberg Retina Tomograph II).
  • No differences were found between normal subjects and those with ocular hypertension in mean retinal nerve fiber layer thickness (0.24/0.24) or between those with ocular hypertension and glaucoma in mean cup depth (0.28/0.3).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Anthropometry / instrumentation. Anthropometry / methods. Diagnosis, Differential. Female. Humans. Intraocular Pressure. Male. Middle Aged. Pupil. Reference Values. Visual Field Tests

  • MedlinePlus Health Information. consumer health - Glaucoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18592440.001).
  • [ISSN] 0365-6691
  • [Journal-full-title] Archivos de la Sociedad Española de Oftalmología
  • [ISO-abbreviation] Arch Soc Esp Oftalmol
  • [Language] spa
  • [Publication-type] Clinical Trial; Comparative Study; English Abstract; Journal Article
  • [Publication-country] Spain
  •  go-up   go-down


16. Kuras A, Baginskas A, Batuleviciene V: Suprathreshold excitation of network of frog tectal neurons by discharging of single retina moving-edge detector. Medicina (Kaunas); 2005;41(11):949-56
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suprathreshold excitation of network of frog tectal neurons by discharging of single retina moving-edge detector.
  • OBJECTIVE: It has been shown that discharge of single darkness detector in the frog retina can lead to suprathreshold excitation of the tectal neurons.
  • MATERIAL AND METHODS: The discharge of a single retina ganglion cell was elicited by the electrical stimulation.
  • RESULTS: The obtained data have suggested that a discharge of a single retinal moving-edge detector elicits a suprathreshold excitation of tectal neurons.
  • [MeSH-major] Neurons / physiology. Retina / physiology. Retinal Ganglion Cells / physiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16333218.001).
  • [ISSN] 1648-9144
  • [Journal-full-title] Medicina (Kaunas, Lithuania)
  • [ISO-abbreviation] Medicina (Kaunas)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Lithuania
  • [Chemical-registry-number] 0 / Excitatory Amino Acid Antagonists; H030S2S85J / Kynurenic Acid
  •  go-up   go-down


17. Lima VM, Piqueira JR, Hanke W: The synergetic modulation of the excitability of central gray matter by a neuropeptide: two protocols using excitation waves in chick retina. An Acad Bras Cienc; 2009 Mar;81(1):39-49
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The synergetic modulation of the excitability of central gray matter by a neuropeptide: two protocols using excitation waves in chick retina.
  • The isolated chick retina provides an in vitro tissue model, in which two protocols were developed to verify the efficacy of a peptide in the excitability control of the central gray matter.
  • [MeSH-major] Membrane Potentials / physiology. Neurons / physiology. Periaqueductal Gray / physiology. Potassium / metabolism. Retina / physiology. Somatostatin / pharmacology

  • MedlinePlus Health Information. consumer health - Potassium.
  • Hazardous Substances Data Bank. POTASSIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19274330.001).
  • [ISSN] 1678-2690
  • [Journal-full-title] Anais da Academia Brasileira de Ciências
  • [ISO-abbreviation] An. Acad. Bras. Cienc.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Chemical-registry-number] 51110-01-1 / Somatostatin; RWP5GA015D / Potassium
  •  go-up   go-down


18. Struik ML, Yazulla S, Kamermans M: Cannabinoid agonist WIN 55212-2 speeds up the cone response to light offset in goldfish retina. Vis Neurosci; 2006 Mar-Apr;23(2):285-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cannabinoid agonist WIN 55212-2 speeds up the cone response to light offset in goldfish retina.
  • These data suggest that a retinal mechanism may account for some of the psychophysical effects of cannabis.
  • Whole-cell patch-clamp recordings were made from cones in the isolated goldfish retina.
  • [MeSH-major] Adaptation, Ocular / physiology. Cannabinoids / agonists. Light. Morpholines / pharmacology. Naphthalenes / pharmacology. Retina / cytology. Retinal Cone Photoreceptor Cells / drug effects

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16638179.001).
  • [ISSN] 0952-5238
  • [Journal-full-title] Visual neuroscience
  • [ISO-abbreviation] Vis. Neurosci.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / R01 EY001682
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzoxazines; 0 / Cannabinoids; 0 / Morpholines; 0 / Naphthalenes; 134959-51-6 / Win 55212-2
  •  go-up   go-down


19. Fischer AJ, Scott MA, Tuten W: Mitogen-activated protein kinase-signaling stimulates Müller glia to proliferate in acutely damaged chicken retina. Glia; 2009 Jan 15;57(2):166-81
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mitogen-activated protein kinase-signaling stimulates Müller glia to proliferate in acutely damaged chicken retina.
  • Müller glia in the mature retina have the capacity to become progenitor-like cells in a many different vertebrate classes.
  • The purpose of this study was to investigate the roles of the Mitogen-Activated Protein Kinase (MAPK) pathway in regulating the activity of Müller glia in the chicken retina.
  • In response to acute retinal damage, we found that Müller glia accumulated phosphorylated ERK1/2 and phospho-CyclicAMP Response Element Binding-protein (pCREB), and transiently expressed immediate early genes, cFos and Egr1, that are known to be downstream of MAPK-signaling.
  • Egr1 and pCREB were normally expressed by retinal progenitors in the circumferential marginal zone (CMZ), whereas cFos and pERK1/2 were not.

  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Dev Biol. 2000 Apr 15;220(2):197-210 [10753510.001]
  • [Cites] J Neurosci. 2000 Nov 15;20(22):RC107 [11069976.001]
  • [Cites] Nat Neurosci. 2001 Mar;4(3):247-52 [11224540.001]
  • [Cites] Exp Eye Res. 2001 May;72(5):495-501 [11311041.001]
  • [Cites] Exp Eye Res. 2001 May;72(5):591-604 [11311051.001]
  • [Cites] Dev Neurosci. 2001;23(4-5):268-76 [11756742.001]
  • [Cites] Development. 2002 May;129(9):2283-91 [11959835.001]
  • [Cites] Brain Behav Evol. 2001;58(5):296-305 [11978947.001]
  • [Cites] J Neurosci. 2002 Nov 1;22(21):9387-98 [12417664.001]
  • [Cites] Glia. 2003 Jul;43(1):70-6 [12761869.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Dec;44(12):5383-95 [14638742.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 2004 May;242(5):414-22 [14963717.001]
  • [Cites] PLoS Biol. 2004 Sep;2(9):E247 [15226823.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 14;101(37):13654-9 [15353594.001]
  • [Cites] J Neurosci. 1992 Oct;12(10):3968-78 [1403094.001]
  • [Cites] J Neurosci. 1994 Mar;14(3 Pt 2):1441-9 [7510332.001]
  • [Cites] J Neurosci. 1995 Nov;15(11):7377-85 [7472491.001]
  • [Cites] Curr Biol. 1996 Jan 1;6(1):16-9 [8805215.001]
  • [Cites] EMBO J. 1996 Sep 2;15(17):4629-42 [8887554.001]
  • [Cites] Dev Genet. 1997;20(3):186-96 [9216059.001]
  • [Cites] J Comp Neurol. 1998 Mar 16;392(3):273-84 [9511918.001]
  • [Cites] J Comp Neurol. 1998 Mar 30;393(1):1-15 [9520096.001]
  • [Cites] Mol Cell Biol. 1998 Apr;18(4):1946-55 [9528766.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1998 Nov;39(12):2427-42 [9804151.001]
  • [Cites] J Comp Neurol. 1999 Mar 1;405(1):1-14 [10022192.001]
  • [Cites] Vision Res. 1999 Feb;39(4):685-97 [10341956.001]
  • [Cites] Nat Neurosci. 1999 Aug;2(8):706-12 [10412059.001]
  • [Cites] Curr Opin Neurobiol. 1999 Oct;9(5):544-53 [10508738.001]
  • [Cites] Mol Cell Neurosci. 2004 Dec;27(4):531-42 [15555930.001]
  • [Cites] Prog Retin Eye Res. 2005 Mar;24(2):161-82 [15610972.001]
  • [Cites] Mol Vis. 2004 Dec 22;10:973-86 [15623987.001]
  • [Cites] J Comp Neurol. 2005 Mar 28;484(1):1-14 [15717308.001]
  • [Cites] Dev Neurosci. 2004;26(5-6):359-70 [15855765.001]
  • [Cites] Development. 2005 Jul;132(13):3015-26 [15944186.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Oct;46(10):3570-7 [16186335.001]
  • [Cites] J Neurosci. 2005 Nov 2;25(44):10157-66 [16267223.001]
  • [Cites] J Comp Neurol. 2006 Jun 1;496(4):479-94 [16572462.001]
  • [Cites] J Neurosci. 2006 Jun 7;26(23):6303-13 [16763038.001]
  • [Cites] Glia. 2006 Aug 1;54(2):94-104 [16710850.001]
  • [Cites] J Neurosci. 2007 Apr 11;27(15):4210-9 [17428999.001]
  • [Cites] J Neurosci. 2007 Jun 27;27(26):7028-40 [17596452.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Nov 16;363(2):347-54 [17880919.001]
  • [Cites] Neurosci Lett. 2007 Oct 29;427(1):55-60 [17920195.001]
  • [Cites] Dev Biol. 2007 Dec 1;312(1):300-11 [18028900.001]
  • [Cites] J Comp Neurol. 2008 Feb 1;506(4):584-603 [18072193.001]
  • [Cites] J Neurosci Res. 2008 Jan;86(1):136-44 [17722069.001]
  • [Cites] J Neurosci. 2008 Jan 30;28(5):1109-17 [18234889.001]
  • [Cites] Brain Res. 2008 Feb 4;1192:76-89 [17320838.001]
  • [Cites] Dev Biol. 2008 May 1;317(1):196-212 [18358467.001]
  • (PMID = 18709648.001).
  • [ISSN] 1098-1136
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY016043-03; United States / NEI NIH HHS / EY / R01 EY016043; United States / NEI NIH HHS / EY / T35 EY007151; United States / NEI NIH HHS / EY / R01 EY016043-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Butadienes; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Early Growth Response Protein 1; 0 / Nitriles; 0 / Proto-Oncogene Proteins c-fos; 0 / Pyrroles; 0 / Receptors, Fibroblast Growth Factor; 0 / SU 5402; 0 / U 0126; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.12.2 / MAP Kinase Kinase 1
  • [Other-IDs] NLM/ NIHMS65202; NLM/ PMC2774719
  •  go-up   go-down


20. Mizuno S, Nishiwaki A, Morita H, Miyake T, Ogura Y: Effects of periocular administration of triamcinolone acetonide on leukocyte-endothelium interactions in the ischemic retina. Invest Ophthalmol Vis Sci; 2007 Jun;48(6):2831-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of periocular administration of triamcinolone acetonide on leukocyte-endothelium interactions in the ischemic retina.
  • PURPOSE: Recent studies have reported that intravitreal or posterior sub-Tenon's injection of triamcinolone acetonide (TA) is effective in the treatment of macular edema resulting from retinal microcirculatory disturbances such as diabetic retinopathy and retinal vein occlusion.
  • The effects of periocular administration of TA on leukocyte-endothelium interactions were studied after transient retinal ischemia.
  • METHODS: Transient retinal ischemia was induced by temporary ligation of the optic nerve sheath for 60 minutes in male Long-Evans rats.
  • Leukocyte dynamics were evaluated in the retinal microcirculation using acridine orange digital fluorography.
  • Also, retinal thickness was studied by using optical coherence tomography and a histologic METHOD: The retinal mRNA expression of P-selectin and intercellular adhesion molecule (ICAM)-1 was semiquantitatively studied with RT-PCR.
  • RESULTS: The leukocytes rolling along retinal vein linings increased after ischemia in the vehicle-treated rats (32.5 +/- 2.1 cells/min).
  • The treatment decreased the retinal thickness and the mRNA expression of P-selectin and ICAM-1.
  • CONCLUSIONS: The present study demonstrated that the periocular injection of TA effectively decreased retinal thickness and inhibited leukocyte-endothelium interactions in the retina after ischemia.
  • Downregulation of adhesion molecules of retinal vascular endothelium induced by TA may play a role in the course.
  • [MeSH-major] Endothelium, Vascular / metabolism. Glucocorticoids / administration & dosage. Ischemia / complications. Leukocytes / metabolism. Macular Edema / drug therapy. Retinal Vessels. Triamcinolone Acetonide / administration & dosage
  • [MeSH-minor] Acridine Orange. Animals. Cell Communication / drug effects. Disease Models, Animal. Fluorescent Dyes. Gene Expression. Injections. Intercellular Adhesion Molecule-1 / genetics. Male. P-Selectin / genetics. RNA, Messenger / metabolism. Rats. Rats, Long-Evans. Retinal Diseases / complications. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Steroids.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17525219.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fluorescent Dyes; 0 / Glucocorticoids; 0 / P-Selectin; 0 / RNA, Messenger; 126547-89-5 / Intercellular Adhesion Molecule-1; F30N4O6XVV / Acridine Orange; F446C597KA / Triamcinolone Acetonide
  •  go-up   go-down


21. Lecchi M, McIntosh JM, Bertrand S, Safran AB, Bertrand D: Functional properties of neuronal nicotinic acetylcholine receptors in the chick retina during development. Eur J Neurosci; 2005 Jun;21(11):3182-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional properties of neuronal nicotinic acetylcholine receptors in the chick retina during development.
  • Acetylcholine (ACh) has been recognized for a long time as a major neurotransmitter in the retina, however, little is known about the contribution of acetylcholine receptors in synaptic processing.
  • To address this question further, we examined the physiological and pharmacological properties of neuronal nicotinic acetylcholine receptors (nAChRs) in retinal ganglion cells from embryonic (E) 12-18-day-old Leghorn chicks.
  • These data demonstrate that ganglion cells of the chick retina express multiple receptor subtypes that progressively develop as a function of retina maturation.
  • [MeSH-major] Cell Differentiation / physiology. Receptors, Nicotinic / metabolism. Retina / embryology. Retinal Ganglion Cells / metabolism. Synapses / metabolism. Synaptic Transmission / physiology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15978026.001).
  • [ISSN] 0953-816X
  • [Journal-full-title] The European journal of neuroscience
  • [ISO-abbreviation] Eur. J. Neurosci.
  • [Language] eng
  • [Grant] United States / NIMH NIH HHS / MH / MH53631
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Bridged Bicyclo Compounds, Heterocyclic; 0 / Conotoxins; 0 / Nicotinic Agonists; 0 / Pyridines; 0 / Receptors, Nicotinic; 0 / alpha-conotoxin MII; 0 / nicotinic receptor alpha3beta2; 0 / nicotinic receptor alpha6; M6K314F1XX / epibatidine; N9YNS0M02X / Acetylcholine
  •  go-up   go-down


22. Setzu A, Lathia JD, Zhao C, Wells K, Rao MS, Ffrench-Constant C, Franklin RJ: Inflammation stimulates myelination by transplanted oligodendrocyte precursor cells. Glia; 2006 Sep;54(4):297-303
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have addressed this issue using a model in which OPCs transplanted into the adult rat retina myelinate retinal ganglion cell axons around the point of injection.
  • Inflammation (characterized by increased expression of the macrophage marker ED1 and the astrocyte marker GFAP, and the up-regulation of multiple cytokines) was induced in the retina by the administration of the TLR-2 ligand zymosan.
  • Myelination, revealed by MBP+ myelin sheaths, was substantially increased when OPCs were injected into the inflamed retina compared to that achieved following transplantation into the normal, noninflamed retina.
  • [MeSH-minor] Animals. Animals, Newborn. Biomarkers. Cell Transplantation / physiology. Cerebral Cortex / cytology. Glial Fibrillary Acidic Protein / metabolism. Immunohistochemistry. Lens, Crystalline / injuries. Ligands. Nerve Fibers / physiology. Oligonucleotide Array Sequence Analysis. Rats. Rats, Inbred F344. Retina / cytology. Toll-Like Receptor 2 / drug effects. Zymosan

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16856149.001).
  • [ISSN] 0894-1491
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] eng
  • [Grant] United Kingdom / Multiple Sclerosis Society / / 689
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Glial Fibrillary Acidic Protein; 0 / Ligands; 0 / Tlr2 protein, rat; 0 / Toll-Like Receptor 2; 9010-72-4 / Zymosan
  •  go-up   go-down


23. Garcá M, Ruiz-Ederra J, Hernández-Barbáchano H, Vecino E: Topography of pig retinal ganglion cells. J Comp Neurol; 2005 Jun 13;486(4):361-72
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Topography of pig retinal ganglion cells.
  • In the present work we analyzed the distribution of retinal ganglion cells (RGCs) in the pig retina.
  • Different regions of the porcine retina were identified following analysis of the distribution of RGCs in terms of cell density and soma size: in the central retina, we found a high-density horizontal RGC band lying dorsal to the optic disc.
  • From the central to the more peripheral retina, we observed a decrease in RGC density, together with a greater presence of RGCs with larger somas.
  • The results of this study should prove to be useful as a foundation for future studies with the porcine retina as a model in ophthalmic research.
  • [MeSH-major] Retina / cytology. Retinal Ganglion Cells / cytology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15846788.001).
  • [ISSN] 0021-9967
  • [Journal-full-title] The Journal of comparative neurology
  • [ISO-abbreviation] J. Comp. Neurol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt; 0 / Stilbamidines
  •  go-up   go-down


24. Hufnagel RB, Le TT, Riesenberg AL, Brown NL: Neurog2 controls the leading edge of neurogenesis in the mammalian retina. Dev Biol; 2010 Apr 15;340(2):490-503
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neurog2 controls the leading edge of neurogenesis in the mammalian retina.
  • In the mammalian retina, neuronal differentiation begins in the dorso-central optic cup and sweeps peripherally and ventrally.
  • In this study, we evaluate the expression and function of proneural bHLH transcription factors during the onset of mouse retinal neurogenesis.
  • Dorso-central retinal progenitor cells that give rise to the first postmitotic neurons express Neurog2/Ngn2 and Atoh7/Math5.
  • However, neurogenesis is eventually restored, and at birth Neurog2 mutant retinas are reduced in size, with only a slight increase in the retinal ganglion cell population.
  • Together, this study supports the hypothesis that the intrinsic factors Neurog2 and Ascl1 regulate the temporal progression of retinal neurogenesis by directing overlapping waves of neuron formation.

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • [Cites] Mol Cell Biol. 2004 Nov;24(21):9517-26 [15485919.001]
  • [Cites] Dev Biol. 1976 Oct 15;53(2):217-40 [825400.001]
  • [Cites] Anat Rec. 1985 Jun;212(2):199-205 [3842042.001]
  • [Cites] Neuron. 1988 Mar;1(1):15-26 [3272153.001]
  • [Cites] Cell Motil Cytoskeleton. 1990;17(2):118-32 [2257630.001]
  • [Cites] Neuron. 1993 Oct;11(4):689-701 [7691107.001]
  • [Cites] Nature. 1994 Jun 2;369(6479):398-400 [8196767.001]
  • [Cites] Cell. 1995 Mar 24;80(6):879-87 [7697718.001]
  • [Cites] Development. 1995 Jul;121(7):2019-30 [7635049.001]
  • [Cites] Exp Neurol. 1995 Jul;134(1):1-12 [7672030.001]
  • [Cites] Development. 1995 Oct;121(10):3267-78 [7588061.001]
  • [Cites] Development. 1995 Nov;121(11):3637-50 [8582277.001]
  • [Cites] Nat Genet. 1996 Apr;12(4):376-84 [8630490.001]
  • [Cites] J Comp Neurol. 1996 May 27;369(2):319-27 [8727003.001]
  • [Cites] J Neurosci. 1997 Feb 15;17(4):1425-34 [9006984.001]
  • [Cites] Development. 1997 Jan;124(2):363-71 [9053312.001]
  • [Cites] Genes Cells. 1996 Aug;1(8):765-74 [9077445.001]
  • [Cites] Neuron. 1997 Nov;19(5):981-94 [9390513.001]
  • [Cites] Neuron. 1998 Mar;20(3):483-94 [9539123.001]
  • [Cites] Development. 1998 Dec;125(23):4821-33 [9806930.001]
  • [Cites] Development. 1999 Jan;126(1):23-36 [9834183.001]
  • [Cites] Dev Biol. 1999 Mar 15;207(2):309-21 [10068465.001]
  • [Cites] Development. 1999 Jul;126(13):2901-9 [10357934.001]
  • [Cites] Development. 1999 Dec;126(24):5713-24 [10572047.001]
  • [Cites] Mol Cell Neurosci. 1999 Oct-Nov;14(4-5):355-69 [10588390.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14996-5001 [10611326.001]
  • [Cites] Genes Dev. 2000 Jan 1;14(1):67-80 [10640277.001]
  • [Cites] Development. 2000 Mar;127(6):1185-96 [10683172.001]
  • [Cites] Dev Biol. 2000 Mar 15;219(2):299-314 [10694424.001]
  • [Cites] Development. 2005 Feb;132(4):829-39 [15677728.001]
  • [Cites] Development. 2005 Apr;132(7):1539-53 [15728672.001]
  • [Cites] Dev Cell. 2005 Apr;8(4):565-74 [15809038.001]
  • [Cites] Development. 2005 Jun;132(11):2573-85 [15857917.001]
  • [Cites] Development. 2005 Jun;132(12):2709-19 [15901662.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Jul;46(7):2540-51 [15980246.001]
  • [Cites] Development. 2005 Sep;132(17):3907-21 [16079155.001]
  • [Cites] Development. 2005 Nov;132(22):4951-62 [16236770.001]
  • [Cites] J Cell Biol. 2005 Dec 19;171(6):991-9 [16365165.001]
  • [Cites] Development. 2006 Feb;133(3):495-505 [16410412.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 31;103(5):1319-24 [16432194.001]
  • [Cites] Dev Neurosci. 2006;28(1-2):128-41 [16508310.001]
  • [Cites] Mol Cell Neurosci. 2006 Mar;31(3):463-9 [16364654.001]
  • [Cites] Genes Dev. 2006 May 1;20(9):1187-202 [16651659.001]
  • [Cites] Cereb Cortex. 2006 Jul;16 Suppl 1:i138-51 [16766700.001]
  • [Cites] Dev Biol. 2006 Jul 15;295(2):764-78 [16690048.001]
  • [Cites] Mol Cell Neurosci. 2007 Dec;36(4):435-48 [17900924.001]
  • [Cites] Mol Cell Neurosci. 2008 Jan;37(1):153-69 [17977745.001]
  • [Cites] J Neurosci. 2008 Jan 16;28(3):749-56 [18199774.001]
  • [Cites] J Neurosci. 2008 Jan 30;28(5):1109-17 [18234889.001]
  • [Cites] Brain Res. 2008 Feb 4;1192:90-8 [17488643.001]
  • [Cites] PLoS One. 2008;3(2):e1588 [18270576.001]
  • [Cites] Dev Biol. 2008 May 15;317(2):560-75 [18417110.001]
  • [Cites] Dev Dyn. 2008 Jun;237(6):1565-80 [18435466.001]
  • [Cites] Nature. 2008 Sep 4;455(7209):114-8 [18690213.001]
  • [Cites] Development. 2008 Oct;135(20):3379-88 [18787067.001]
  • [Cites] BMC Dev Biol. 2008;8:101 [18854032.001]
  • [Cites] Dev Biol. 2009 Feb 15;326(2):471-81 [19059393.001]
  • [Cites] Dev Dyn. 2009 Feb;238(2):451-8 [19161242.001]
  • [Cites] Mol Cell Neurosci. 2009 Feb;40(2):187-98 [19028584.001]
  • [Cites] Genesis. 2009 Mar;47(3):175-87 [19208436.001]
  • [Cites] Development. 2009 Nov;136(22):3767-77 [19855019.001]
  • [Cites] Mol Cell Neurosci. 2009 Dec;42(4):267-77 [19646530.001]
  • [Cites] J Neurobiol. 2000 Feb 5;42(2):232-47 [10640330.001]
  • [Cites] Development. 2000 Jul;127(14):3021-30 [10862740.001]
  • [Cites] Neuron. 2000 Aug;27(2):193-5 [10985338.001]
  • [Cites] Neuron. 2000 Aug;27(2):251-63 [10985346.001]
  • [Cites] Science. 2000 Sep 22;289(5487):2137-9 [11000118.001]
  • [Cites] Development. 2000 Oct;127(20):4325-34 [11003833.001]
  • [Cites] Genes Dev. 2001 Jan 1;15(1):24-9 [11156601.001]
  • [Cites] Development. 2001 Jan;128(2):217-31 [11124117.001]
  • [Cites] Development. 2001 Apr;128(8):1313-22 [11262232.001]
  • [Cites] Cell. 2001 Apr 6;105(1):43-55 [11301001.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2001 May;42(6):1312-8 [11328745.001]
  • [Cites] J Neurosci. 2001 Jun 15;21(12):4259-71 [11404411.001]
  • [Cites] Neuron. 2001 Jun;30(3):725-36 [11430806.001]
  • [Cites] Development. 2001 Jul;128(13):2497-508 [11493566.001]
  • [Cites] Neuron. 2001 Aug 2;31(2):219-32 [11502254.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15014-9 [11752450.001]
  • [Cites] Genes Dev. 2002 Feb 1;16(3):324-38 [11825874.001]
  • [Cites] Development. 2002 Feb;129(4):831-42 [11861467.001]
  • [Cites] Development. 2002 Apr;129(7):1553-67 [11923194.001]
  • [Cites] Development. 2003 Apr;130(8):1565-77 [12620982.001]
  • [Cites] Nat Genet. 2003 May;34(1):53-8 [12692551.001]
  • [Cites] Development. 2003 Jul;130(13):2903-15 [12756174.001]
  • [Cites] Neuron. 2003 Jul 31;39(3):439-52 [12895419.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Jan;45(1):48-58 [14691153.001]
  • [Cites] J Biol Chem. 2004 Jul 2;279(27):28492-8 [15105417.001]
  • (PMID = 20144606.001).
  • [ISSN] 1095-564X
  • [Journal-full-title] Developmental biology
  • [ISO-abbreviation] Dev. Biol.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY013612-09A1; United States / NEI NIH HHS / EY / R01 EY013612-09A1; United States / NEI NIH HHS / EY / R01 EY018097; United States / NEI NIH HHS / EY / R01 EY013612; United States / NEI NIH HHS / EY / EY13612; United States / NEI NIH HHS / EY / EY18097
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Nerve Tissue Proteins; 0 / Neurog2 protein, mouse; 147336-22-9 / Green Fluorescent Proteins; EC 3.2.1.23 / beta-Galactosidase
  • [Other-IDs] NLM/ NIHMS178692; NLM/ PMC2854206
  •  go-up   go-down


25. Surace EM, Auricchio A: Versatility of AAV vectors for retinal gene transfer. Vision Res; 2008 Feb;48(3):353-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Versatility of AAV vectors for retinal gene transfer.
  • Gene therapy represents a promising therapeutic option for many inherited and acquired retinal diseases.
  • Recombinant adeno-associated viral vectors (AAV) are the most efficient tools to transfer genes in vivo to the retina.
  • The results from the forthcoming trials with AAV in the retina of patients with Leber Congenital Amaurosis will be critical for the rapid development of AAV-based therapeutics for retinal diseases.
  • [MeSH-major] Dependovirus / genetics. Eye Diseases, Hereditary / therapy. Gene Transfer Techniques. Genetic Vectors. Retinal Diseases / therapy

  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17923143.001).
  • [ISSN] 0042-6989
  • [Journal-full-title] Vision research
  • [ISO-abbreviation] Vision Res.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / R01 EY015136; Italy / Telethon / / TGM06C03; Italy / Telethon / / TGM06S01; United States / NEI NIH HHS / EY / 1R01EY015136-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 104
  •  go-up   go-down


26. Duan L, Zhang MX: [Effects of endostatin on the expression of Tubulinbeta mRNA in the retina of oxygen-induced retinal neovascularization]. Sichuan Da Xue Xue Bao Yi Xue Ban; 2009 Nov;40(6):1008-10, 1020
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effects of endostatin on the expression of Tubulinbeta mRNA in the retina of oxygen-induced retinal neovascularization].
  • OBJECTIVE: To investigate the effect of endostatin on the expression of Tubulinbeta in the retina of oxygen-induced retinal neovascularization.
  • In control group, the mice were bred in normal oxygen condition, while the mice in another 2 groups were subjected to hyperoxia condition to establish the oxygen-induced retinal neovascularization model.
  • Total RNA were extracted from retina of each mouse in three groups, the quantity of Tubulinbeta mRNA in retina was analyzed with quantitative real-time PCR with the special primers.
  • RESULTS: Quantitativereal-time PCR results indicated that, the expression of Tubulinbeta mRNA in retica was up-regulated in the process of retinal neovascularization induced by hyperoxia, and down-regulated by the treatment of ES.
  • CONCLUSIONS: Endotatin can inhibit the expression of Tubulinbeta mRNA in retinal neovascularization, this may be correlated with the inhibitive characteristics of ES on neovascularization.
  • [MeSH-major] Endostatins / pharmacology. Hyperoxia / metabolism. Retina / metabolism. Retinal Neovascularization / metabolism. Tubulin / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20067108.001).
  • [ISSN] 1672-173X
  • [Journal-full-title] Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition
  • [ISO-abbreviation] Sichuan Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Endostatins; 0 / RNA, Messenger; 0 / Tubulin; 0 / beta3 tubulin, mouse
  •  go-up   go-down


27. Wolfe AD, Henry JJ: Neuronal leucine-rich repeat 6 (XlNLRR-6) is required for late lens and retina development in Xenopus laevis. Dev Dyn; 2006 Apr;235(4):1027-41
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuronal leucine-rich repeat 6 (XlNLRR-6) is required for late lens and retina development in Xenopus laevis.
  • Using antisense morpholino oligonucleotide (MO) -mediated knockdown of XlNLRR-6, we demonstrate that this protein is critical for development of the lens, retina, and cornea.
  • Reciprocal transplantation of presumptive lens ectoderm between MO-treated and untreated embryos demonstrate that XlNLRR-6 plays autonomous roles in the development of both the lens and retina.
  • [MeSH-major] Gene Expression Regulation, Developmental. Lens, Crystalline / embryology. Leucine. Neurons / metabolism. Retina / embryology. Xenopus laevis / embryology

  • Hazardous Substances Data Bank. L-Leucine .
  • Xenbase. Xenbase .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16456849.001).
  • [ISSN] 1058-8388
  • [Journal-full-title] Developmental dynamics : an official publication of the American Association of Anatomists
  • [ISO-abbreviation] Dev. Dyn.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY 09844
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oligonucleotides, Antisense; 0 / Xenopus Proteins; GMW67QNF9C / Leucine
  •  go-up   go-down


28. Curto GG, Lara JM, Parrilla M, Aijón J, Velasco A: Modifications of the retina neuronal populations of the heterozygous mutant small eye mouse, the Sey(Dey). Brain Res; 2007 Jan 5;1127(1):163-76
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modifications of the retina neuronal populations of the heterozygous mutant small eye mouse, the Sey(Dey).
  • We analyzed the modifications of the retinal neurons in a heterozygous mutant small eye mouse, the Sey(Dey).
  • The partial loss of the genes affected does not prevent the formation of the different layers of the retina, but does affect its thickness, principally of the plexiform layers; moreover, the internal limiting membrane is found disorganized.
  • All the neuronal populations are present in the retina of these animals and express the same neurochemical markers as the control animals, but the number of Pax6(+) cells is notably reduced.
  • These results suggest that, although it does not appear determinant in the differentiation of the distinct neuronal types of the retina, the partial lack of genes of the heterozygotes +/Sey(Dey) provokes important morphological and neurochemical modifications in the cytoarchitecture of the retina.
  • [MeSH-major] Eye Abnormalities / pathology. Eye Proteins / genetics. Gene Expression Regulation, Developmental / genetics. Homeodomain Proteins / genetics. Mutation / genetics. Neurons / pathology. Paired Box Transcription Factors / genetics. Repressor Proteins / genetics. Retina / abnormalities
  • [MeSH-minor] Animals. Axons / metabolism. Axons / pathology. Biomarkers / metabolism. Calbindin 2. Calbindins. Calcium-Binding Proteins / genetics. Cell Differentiation / genetics. Dendrites / metabolism. Dendrites / pathology. Disease Models, Animal. Female. Male. Mice. Mice, Neurologic Mutants. Parvalbumins / genetics. Protein Kinase C-alpha / genetics. Retinal Ganglion Cells / metabolism. Retinal Ganglion Cells / pathology. S100 Calcium Binding Protein G / genetics. Tyrosine 3-Monooxygenase / genetics. WT1 Proteins / genetics

  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17113047.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Calbindin 2; 0 / Calbindins; 0 / Calcium-Binding Proteins; 0 / Eye Proteins; 0 / Homeodomain Proteins; 0 / PAX6 protein; 0 / Paired Box Transcription Factors; 0 / Parvalbumins; 0 / Repressor Proteins; 0 / S100 Calcium Binding Protein G; 0 / WT1 Proteins; 148998-28-1 / reticulocalbin; EC 1.14.16.2 / Tyrosine 3-Monooxygenase; EC 2.7.11.13 / Protein Kinase C-alpha
  •  go-up   go-down


29. Hasegawa T, McLeod DS, Prow T, Merges C, Grebe R, Lutty GA: Vascular precursors in developing human retina. Invest Ophthalmol Vis Sci; 2008 May;49(5):2178-92
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vascular precursors in developing human retina.
  • PURPOSE: Prior investigation has demonstrated that angioblasts are present in the inner retinas of human embryos and fetuses and that they differentiate and organize to form the primordial retinal vasculature.
  • Coexpression of CD39 (marker for retinal angioblasts and endothelial cells) and CXCR4 or c-Kit was investigated by confocal microscopy.
  • RESULTS: SDF-1 was prominent in inner retina with the greatest reaction product near the internal limiting membrane (ILM).
  • SCF immunoreactivity was also confined to the inner retina and increased significantly between 7 and 12 WG.
  • A layer of CXCR4(+) and c-Kit(+) precursors, some of which coexpressed CD39, existed in the inner retina from 7 to 12 WG.
  • CONCLUSIONS: Embryonic human retina has a pool of precursors (CXCR4(+) and c-Kit(+)) that enlarged centrifugally during fetal development.
  • Both SCF and SDF-1 are associated with the differentiation of retinal precursors into angioblasts and their migration to sites of vessel assembly.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Invest Ophthalmol Vis Sci. 2008 Jun;49(6):2342
  • (PMID = 18436851.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY 01765; United States / NEI NIH HHS / EY / P30 EY001765; United States / NEI NIH HHS / EY / EY 09357; United States / NEI NIH HHS / EY / R01 EY009357; United States / NEI NIH HHS / EY / R01 EY009357-16
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / CXCR4 protein, human; 0 / Chemokine CXCL12; 0 / Receptors, CXCR4; 0 / Stem Cell Factor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 3.6.1.5 / Apyrase; EC 3.6.1.5 / CD39 antigen
  • [Other-IDs] NLM/ NIHMS215629; NLM/ PMC4943084
  •  go-up   go-down


30. Weber AJ, Harman CD: BDNF preserves the dendritic morphology of alpha and beta ganglion cells in the cat retina after optic nerve injury. Invest Ophthalmol Vis Sci; 2008 Jun;49(6):2456-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BDNF preserves the dendritic morphology of alpha and beta ganglion cells in the cat retina after optic nerve injury.
  • PURPOSE: To examine whether brain-derived neurotrophic factor (BDNF), a potent neuroprotectant in the mammalian retina, also plays a role in preserving the dendritic integrity of the surviving ganglion cells after optic nerve injury.
  • [MeSH-major] Brain-Derived Neurotrophic Factor / pharmacology. Dendrites / drug effects. Neuroprotective Agents / pharmacology. Optic Nerve Injuries / drug therapy. Retinal Ganglion Cells / drug effects
  • [MeSH-minor] Animals. Cats. Cell Count. Cell Survival / drug effects. Recombinant Proteins / pharmacology. Retinal Degeneration / etiology. Retinal Degeneration / prevention & control

  • MedlinePlus Health Information. consumer health - Optic Nerve Disorders.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18263808.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY11159
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Brain-Derived Neurotrophic Factor; 0 / Neuroprotective Agents; 0 / Recombinant Proteins
  •  go-up   go-down


31. Natoli R, Provis J, Valter K, Stone J: Expression and role of the early-response gene Oxr1 in the hyperoxia-challenged mouse retina. Invest Ophthalmol Vis Sci; 2008 Oct;49(10):4561-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression and role of the early-response gene Oxr1 in the hyperoxia-challenged mouse retina.
  • PURPOSE: To examine the response of mouse retina to sustained hyperoxia.
  • RESULTS: In the C57BL/6J retina, Oxr1 was upregulated at 3 days of exposure, matching the early period of resistance to hyperoxia in this strain, and fell below control levels at 14 days, when photoreceptor degeneration had begun.
  • The retinal response to hyperoxia may constitute acute and chronic phases in which photoreceptors are first resistant, and then vulnerable, to oxidative damage.
  • Understanding this biphasic response may be important in understanding the role of oxygen in the progress of retinal dystrophy.
  • [MeSH-major] Gene Expression Regulation / physiology. Hyperoxia / genetics. Nuclear Proteins / genetics. Oxidative Stress. Oxygen / toxicity. Photoreceptor Cells, Vertebrate / metabolism. Retinal Degeneration / genetics

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. OXYGEN .
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18539939.001).
  • [ISSN] 1552-5783
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Fibrillary Acidic Protein; 0 / Mitochondrial Proteins; 0 / Nuclear Proteins; 0 / Oxr1 protein, mouse; 0 / RNA, Messenger; S88TT14065 / Oxygen
  •  go-up   go-down


32. Haynes T, Gutierrez C, Aycinena JC, Tsonis PA, Del Rio-Tsonis K: BMP signaling mediates stem/progenitor cell-induced retina regeneration. Proc Natl Acad Sci U S A; 2007 Dec 18;104(51):20380-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BMP signaling mediates stem/progenitor cell-induced retina regeneration.
  • We identified a mechanism whereby retina regeneration in the embryonic chick can be induced by the contribution of stem/progenitor cells.
  • We show that bone morphogenetic protein (BMP) signaling is sufficient and necessary to induce retina regeneration and that its action can be divided into two phases.
  • These results unravel a mechanism for stem/progenitor cell-mediated retina regeneration, where BMP activation establishes a cross-talk with the FGF pathway and selectively activates the canonical and noncanonical BMP pathways.
  • Retina stem/progenitor cells exist in other species, including humans.
  • Thus, our findings provide insights on how retinal stem cells can be activated for possible regenerative therapies.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2000 Jun 9;275(23):17647-52 [10748100.001]
  • [Cites] Dev Dyn. 2007 May;236(5):1161-74 [17385725.001]
  • [Cites] J Neurosci. 2001 Feb 15;21(4):1292-301 [11160400.001]
  • [Cites] Development. 2002 Jul;129(13):3161-71 [12070091.001]
  • [Cites] Dev Biol. 2002 Oct 15;250(2):231-50 [12376100.001]
  • [Cites] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886.001]
  • [Cites] Dev Biol. 2003 Apr 1;256(1):34-48 [12654290.001]
  • [Cites] Cell Signal. 2004 Mar;16(3):291-9 [14687659.001]
  • [Cites] Exp Eye Res. 2004 Feb;78(2):161-72 [14729349.001]
  • [Cites] Development. 2004 Sep;131(18):4607-21 [15342484.001]
  • [Cites] Dev Biol. 1989 Jul;134(1):201-5 [2731647.001]
  • [Cites] Dev Dyn. 1997 Mar;208(3):349-62 [9056639.001]
  • [Cites] Development. 1997 Jun;124(11):2203-12 [9187146.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1997 Jun;38(7):1293-303 [9191592.001]
  • [Cites] Genes Dev. 1997 Sep 1;11(17):2191-203 [9303535.001]
  • [Cites] Dev Biol. 1999 Mar 1;207(1):176-88 [10049573.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Nov 2;101(44):15772-7 [15505221.001]
  • [Cites] Int J Dev Biol. 2004;48(8-9):965-74 [15558487.001]
  • [Cites] Development. 2005 Mar;132(5):913-23 [15673568.001]
  • [Cites] Cytokine Growth Factor Rev. 2005 Apr;16(2):139-49 [15863030.001]
  • [Cites] Dev Biol. 2005 Jul 15;283(2):335-44 [15907833.001]
  • [Cites] Mol Cell Biol. 2005 Sep;25(17):7711-24 [16107717.001]
  • [Cites] Curr Neurovasc Res. 2004 Jul;1(3):231-9 [16181073.001]
  • [Cites] J Comp Neurol. 2006 Mar 20;495(3):263-78 [16440295.001]
  • [Cites] J Comp Neurol. 2001 Feb 19;430(4):562-72 [11169487.001]
  • (PMID = 18093961.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R21 AG024937-02; United States / NIA NIH HHS / AG / R21 AG 024937-01; United States / NIA NIH HHS / AG / AG024937-02; United States / NEI NIH HHS / EY / EY10540; United States / NEI NIH HHS / EY / R01 EY010540; United States / NIA NIH HHS / AG / R21 AG024937
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Morphogenetic Proteins; 0 / Smad Proteins; 62031-54-3 / Fibroblast Growth Factors; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC2154439
  •  go-up   go-down


33. Subramanian P, Notario PM, Becerra SP: Pigment epithelium-derived factor receptor (PEDF-R): a plasma membrane-linked phospholipase with PEDF binding affinity. Adv Exp Med Biol; 2010;664:29-37
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pigment epithelium-derived factor (PEDF), a multifunctional protein, acts in retinal differentiation, survival and maintenance by interacting with high affinity receptors on the surface of target cells.
  • This newly identified protein is present on the surface of retina and RPE cells, and has the expected transmembrane topology.
  • In summary, PEDF-R is a novel component of the retina that is a phospholipase-linked membrane protein with high affinity for PEDF.
  • [MeSH-minor] Computational Biology. Humans. Ligands. Protein Binding. Protein Transport. Retina / cytology. Retina / enzymology. Subcellular Fractions / enzymology

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 1999 Oct 29;274(44):31605-12 [10531367.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Oct;44(10):4497-504 [14507898.001]
  • [Cites] Exp Eye Res. 2004 Feb;78(2):223-34 [14729355.001]
  • [Cites] Am J Ophthalmol. 2004 Apr;137(4):668-74 [15059706.001]
  • [Cites] Am J Ophthalmol. 2004 Jun;137(6):1129-30 [15183804.001]
  • [Cites] Prog Retin Eye Res. 2004 Sep;23(5):561-77 [15302351.001]
  • [Cites] Exp Eye Res. 1991 Sep;53(3):411-4 [1936177.001]
  • [Cites] J Neurosci. 1995 Jul;15(7 Pt 1):4992-5003 [7623128.001]
  • [Cites] Protein Expr Purif. 1995 Aug;6(4):447-56 [8527930.001]
  • [Cites] Mol Vis. 1998 Apr 20;4:7 [9565647.001]
  • [Cites] Biochim Biophys Acta. 1998 Jun 16;1398(2):203-14 [9689919.001]
  • [Cites] Science. 1999 Jul 9;285(5425):245-8 [10398599.001]
  • [Cites] J Neuropathol Exp Neurol. 1999 Jul;58(7):719-28 [10411342.001]
  • [Cites] J Biol Chem. 2004 Nov 19;279(47):48968-75 [15364929.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D447-53 [15608235.001]
  • [Cites] Brain Pathol. 2005 Apr;15(2):159-66 [15912889.001]
  • [Cites] Retina. 2005 Dec;25(8 Suppl):S29-S30 [16374323.001]
  • [Cites] EMBO Rep. 2006 Jan;7(1):106-13 [16239926.001]
  • [Cites] Exp Eye Res. 2006 May;82(5):739-40 [16364294.001]
  • [Cites] J Biol Chem. 2006 Dec 8;281(49):38022-37 [17032652.001]
  • [Cites] Am J Pathol. 2008 Nov;173(5):1326-38 [18845835.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2001 Jun;42(7):1646-52 [11381073.001]
  • [Cites] Eur J Biochem. 2001 Oct;268(19):5037-44 [11589694.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2001 Dec;42(13):3287-93 [11726635.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Mar;43(3):821-9 [11867604.001]
  • [Cites] Trends Mol Med. 2002 Jul;8(7):330-4 [12114112.001]
  • [Cites] Am J Ophthalmol. 2002 Aug;134(2):220-7 [12140029.001]
  • [Cites] Biochemistry. 2003 Jun 10;42(22):6696-708 [12779324.001]
  • [Cites] Lipids. 2003 Jun;38(6):677-82 [12934679.001]
  • [Cites] Neurobiol Dis. 1999 Dec;6(6):523-32 [10600408.001]
  • (PMID = 20237999.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 EY000306-13
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Eye Proteins; 0 / Ligands; 0 / Nerve Growth Factors; 0 / Receptors, Neuropeptide; 0 / Serpins; 0 / pigment epithelium-derived factor; 0 / pigment epithelium-derived factor receptor; EC 3.1.- / Phospholipases
  • [Other-IDs] NLM/ NIHMS544292; NLM/ PMC3901638
  •  go-up   go-down


34. Katyal S, Gao Z, Monckton E, Glubrecht D, Godbout R: Hierarchical disabled-1 tyrosine phosphorylation in Src family kinase activation and neurite formation. J Mol Biol; 2007 Apr 27;368(2):349-64
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There are two developmentally regulated alternatively spliced forms of Disabled-1 (Dab1) in the chick retina: an early form (Dab1-E) expressed in retinal precursor cells and a late form (Dab1-L) expressed in neuronal cells.
  • Here, we use Reelin-expressing primary retinal cultures to investigate the role of the four Dab1 tyrosine phosphorylation sites on overall tyrosine phosphorylation, Dab1 phosphorylation, SFK activation and neurite formation.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosci. 2006 Feb 8;26(6):1767-75 [16467525.001]
  • [Cites] J Neurosci. 2005 Sep 14;25(37):8578-86 [16162939.001]
  • [Cites] J Comp Neurol. 2000 Aug 21;424(2):327-38 [10906706.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 15;97(17):9729-34 [10920200.001]
  • [Cites] Curr Biol. 2000 Jul 27-Aug 10;10(15):877-85 [10959835.001]
  • [Cites] Nat Cell Biol. 2000 Nov;2(11):767-75 [11056530.001]
  • [Cites] J Biol Chem. 2001 May 11;276(19):16008-14 [11279201.001]
  • [Cites] Neuron. 2001 Sep 27;31(6):929-41 [11580894.001]
  • [Cites] Neuron. 2002 Feb 14;33(4):573-86 [11856531.001]
  • [Cites] Methods Enzymol. 2002;350:199-218 [12073313.001]
  • [Cites] J Biol Chem. 2002 Dec 20;277(51):49958-64 [12376533.001]
  • [Cites] Curr Biol. 2003 Jan 8;13(1):9-17 [12526739.001]
  • [Cites] Curr Biol. 2003 Jan 8;13(1):18-26 [12526740.001]
  • [Cites] Nat Rev Neurosci. 2003 Jun;4(6):496-505 [12778121.001]
  • [Cites] Mol Cell Biol. 2003 Oct;23(20):7210-21 [14517291.001]
  • [Cites] Brain Res Mol Brain Res. 2003 Oct 7;117(2):152-9 [14559149.001]
  • [Cites] Nat Genet. 2003 Nov;35(3):270-6 [14578885.001]
  • [Cites] Neuron. 2004 Jan 8;41(1):71-84 [14715136.001]
  • [Cites] Mol Cell Biol. 2004 Feb;24(3):1378-86 [14729980.001]
  • [Cites] J Comp Neurol. 2004 Mar 15;470(4):372-81 [14961563.001]
  • [Cites] Curr Biol. 2004 Apr 6;14(7):606-10 [15062102.001]
  • [Cites] Neuron. 2004 Apr 22;42(2):197-211 [15091337.001]
  • [Cites] EMBO J. 2004 Apr 21;23(8):1878-88 [15057276.001]
  • [Cites] J Cell Sci. 2004 Sep 1;117(Pt 19):4527-36 [15316068.001]
  • [Cites] Brain Res. 1983 Oct;312(1):21-32 [6652506.001]
  • [Cites] Cell. 1993 Mar 12;72(5):767-78 [7680959.001]
  • [Cites] Nature. 1995 Apr 20;374(6524):719-23 [7715726.001]
  • [Cites] Neuron. 1995 May;14(5):899-912 [7748558.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 23;93(2):589-95 [8570600.001]
  • [Cites] J Neurosci. 1997 Jan 1;17(1):23-31 [8987733.001]
  • [Cites] EMBO J. 1997 Jan 2;16(1):121-32 [9009273.001]
  • [Cites] Neuron. 1997 Aug;19(2):239-49 [9292716.001]
  • [Cites] Nature. 1997 Oct 16;389(6652):730-3 [9338784.001]
  • [Cites] Mol Vis. 1999 Apr 19;5:4 [10209197.001]
  • [Cites] Cell. 1999 Jun 11;97(6):689-701 [10380922.001]
  • [Cites] Curr Eye Res. 1999 Jul;19(1):66-75 [10415459.001]
  • [Cites] Neuron. 1999 Oct;24(2):481-9 [10571241.001]
  • (PMID = 17350651.001).
  • [ISSN] 0022-2836
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] ENG
  • [Grant] None / None / / 82789-1; Canada / Canadian Institutes of Health Research / / 82789-1
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Avian Proteins; 0 / Cell Adhesion Molecules, Neuronal; 0 / Extracellular Matrix Proteins; 0 / Nerve Tissue Proteins; 0 / Protein Isoforms; 0 / Receptors, LDL; 0 / Recombinant Fusion Proteins; 0 / VLDL receptor; 147336-22-9 / Green Fluorescent Proteins; 21820-51-9 / Phosphotyrosine; EC 2.7.10.2 / src-Family Kinases; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / reelin protein
  • [Other-IDs] NLM/ CAMS3217; NLM/ PMC4071145
  •  go-up   go-down


35. Oh EC, Khan N, Novelli E, Khanna H, Strettoi E, Swaroop A: Transformation of cone precursors to functional rod photoreceptors by bZIP transcription factor NRL. Proc Natl Acad Sci U S A; 2007 Jan 30;104(5):1679-84
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Networks of transcriptional regulatory proteins dictate specification of neural lineages from multipotent retinal progenitors.
  • To examine the role of NRL in cell fate determination, we generated transgenic mice that express Nrl under the control of Crx promoter in postmitotic photoreceptor precursors of WT and Nrl-/- retina.
  • We show that NRL expression, in both genetic backgrounds, leads to a functional retina with only rod photoreceptors.
  • The absence of cones does not alter retinal lamination, although cone synaptic circuitry is now recruited by rods.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2003 Jul 24;424(6947):426-30 [12879070.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):191-5 [8552602.001]
  • [Cites] Nat Neurosci. 2003 Dec;6(12):1255-63 [14625556.001]
  • [Cites] Neuron. 2003 Dec 4;40(5):897-904 [14659089.001]
  • [Cites] J Comp Neurol. 2004 Jan 26;469(1):70-82 [14689473.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Jan;45(1):42-7 [14691152.001]
  • [Cites] J Neurosci. 2000 Mar 15;20(6):2247-54 [10704500.001]
  • [Cites] Cell Mol Life Sci. 2000 Feb;57(2):224-34 [10766019.001]
  • [Cites] Cell. 2000 May 26;101(5):485-98 [10850491.001]
  • [Cites] J Biol Chem. 2000 Sep 22;275(38):29794-9 [10887186.001]
  • [Cites] Nat Genet. 2001 Jan;27(1):94-8 [11138006.001]
  • [Cites] Nat Rev Neurosci. 2001 Feb;2(2):109-18 [11252990.001]
  • [Cites] Cell. 2001 Apr 6;105(1):43-55 [11301001.001]
  • [Cites] J Biol Chem. 2001 Sep 14;276(37):34999-5007 [11438531.001]
  • [Cites] Mol Ther. 2004 Feb;9(2):182-8 [14759802.001]
  • [Cites] Curr Opin Neurobiol. 2004 Feb;14(1):15-21 [15018933.001]
  • [Cites] Semin Cell Dev Biol. 2004 Feb;15(1):83-9 [15036211.001]
  • [Cites] J Biol Chem. 2001 Sep 28;276(39):36824-30 [11477108.001]
  • [Cites] Nat Genet. 2001 Dec;29(4):447-52 [11694879.001]
  • [Cites] J Neurosci. 2002 Mar 1;22(5):1640-7 [11880494.001]
  • [Cites] J Neurosci. 2002 Jul 1;22(13):5492-504 [12097501.001]
  • [Cites] Hum Mol Genet. 2003 Feb 15;12(4):365-73 [12566383.001]
  • [Cites] Nat Genet. 2003 May;34(1):53-8 [12692551.001]
  • [Cites] Nature. 2003 Jul 10;424(6945):147-51 [12853946.001]
  • [Cites] Hum Mol Genet. 2004 May 15;13(10):1025-40 [15028672.001]
  • [Cites] J Biol Chem. 2004 May 7;279(19):19800-7 [15001570.001]
  • [Cites] J Comp Neurol. 2004 Jun 21;474(2):304-24 [15164429.001]
  • [Cites] Hum Mol Genet. 2004 Jul 15;13(14):1487-503 [15163632.001]
  • [Cites] Hum Mol Genet. 2004 Aug 1;13(15):1563-75 [15190009.001]
  • [Cites] J Comp Neurol. 2004 Aug 23;476(3):254-66 [15269969.001]
  • [Cites] J Neurosci. 2004 Aug 25;24(34):7576-82 [15329405.001]
  • [Cites] J Biol Chem. 2004 Oct 1;279(40):42211-20 [15292180.001]
  • [Cites] J Comp Neurol. 1979 Nov 15;188(2):245-62 [500858.001]
  • [Cites] J Comp Neurol. 1979 Nov 15;188(2):263-72 [500859.001]
  • [Cites] Anat Rec. 1985 Jun;212(2):199-205 [3842042.001]
  • [Cites] Science. 1988 Mar 4;239(4844):1142-5 [2449732.001]
  • [Cites] Science. 1989 Jan 20;243(4889):391-3 [2911751.001]
  • [Cites] Neuron. 1990 Jun;4(6):833-45 [2163263.001]
  • [Cites] Development. 1992 Apr;114(4):899-906 [1618151.001]
  • [Cites] J Comp Neurol. 1993 May 22;331(4):564-77 [8509512.001]
  • [Cites] Vis Neurosci. 1994 Jul-Aug;11(4):773-80 [7918227.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 23;93(2):589-95 [8570600.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 30;93(9):3920-5 [8632990.001]
  • [Cites] Science. 1996 Nov 15;274(5290):1133-8 [8895456.001]
  • [Cites] Development. 1997 Mar;124(5):1055-67 [9056780.001]
  • [Cites] Neuron. 1997 Nov;19(5):1017-30 [9390516.001]
  • [Cites] Cell. 1998 Oct 30;95(3):393-407 [9814709.001]
  • [Cites] Cell. 1999 Jan 22;96(2):211-24 [9988216.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Nov 2;101(44):15772-7 [15505221.001]
  • [Cites] J Neurosci. 2005 Jan 5;25(1):118-29 [15634773.001]
  • [Cites] Hum Mol Genet. 2005 Mar 15;14(6):747-64 [15689355.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Jun;46(6):2156-67 [15914637.001]
  • [Cites] Stem Cells. 2006 Feb;24(2):246-57 [16123388.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 7;103(10):3890-5 [16505381.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 18;103(16):6218-23 [16606843.001]
  • [Cites] Nat Neurosci. 2006 Jun;9(6):743-51 [16680166.001]
  • [Cites] Mol Endocrinol. 2006 Aug;20(8):1728-41 [16574740.001]
  • [Cites] Hum Mol Genet. 2006 Sep 1;15(17):2588-602 [16868010.001]
  • [Cites] J Biol Chem. 2006 Sep 15;281(37):27327-34 [16854989.001]
  • [Cites] Nature. 2006 Nov 9;444(7116):203-7 [17093405.001]
  • [Cites] Nature. 2003 Jul 24;424(6947):430-4 [12879071.001]
  • (PMID = 17242361.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY007003; United States / NEI NIH HHS / EY / R01 EY012654; United States / NEI NIH HHS / EY / R01 EY011115; United States / NIDDK NIH HHS / DK / P60 DK020572; United States / NEI NIH HHS / EY / EY012654; United States / NEI NIH HHS / EY / EY011115; United States / NIDDK NIH HHS / DK / 5P60 DK20572; United States / NEI NIH HHS / EY / P30 EY007003; United States / NEI NIH HHS / EY / F31 EY007003
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic-Leucine Zipper Transcription Factors; 0 / Eye Proteins; 0 / Nrl protein, mouse
  • [Other-IDs] NLM/ PMC1780067
  •  go-up   go-down


36. Majumdar S, Wässle H, Jusuf PR, Haverkamp S: Mirror-symmetrical populations of wide-field amacrine cells of the macaque monkey retina. J Comp Neurol; 2008 May 1;508(1):13-27
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mirror-symmetrical populations of wide-field amacrine cells of the macaque monkey retina.
  • The density of the cells increased from approximately 70/mm(2) in the peripheral retina to approximately 700/mm(2) in the central retina.
  • The close proximity of the dendritic strata of glypho-immunoreactive amacrine cells, cholinergic amacrine cells, and direction-selective ganglion cells suggests a possible role of the cells in the generation of direction-selective light responses of the monkey retina.
  • [MeSH-major] Amacrine Cells. Macaca fascicularis / anatomy & histology. Retina / cytology

  • COS Scholar Universe. author profiles.
  • SciCrunch. The Antibody Registry: Reagent: Antibodies .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18288700.001).
  • [ISSN] 1096-9861
  • [Journal-full-title] The Journal of comparative neurology
  • [ISO-abbreviation] J. Comp. Neurol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids; 0 / dolaisoleucine; 56-12-2 / gamma-Aminobutyric Acid; EC 2.3.1.6 / Choline O-Acetyltransferase; EC 2.4.1.- / Glycogen Phosphorylase
  •  go-up   go-down


37. Katsumata O, Ohara N, Tamaki H, Niimura T, Naganuma H, Watanabe M, Sakagami H: IQ-ArfGEF/BRAG1 is associated with synaptic ribbons in the mouse retina. Eur J Neurosci; 2009 Oct;30(8):1509-16
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IQ-ArfGEF/BRAG1 is associated with synaptic ribbons in the mouse retina.
  • In this study, we examined the immunohistochemical localization of IQ-ArfGEF/BRAG1 in the adult mouse retina using light and electron microscopy.
  • Furthermore, immunoprecipitation analysis showed that anti-IQ-ArfGEF/BRAG1 antibody efficiently pulled down RIBEYE from retinal lysates.
  • These findings indicate that IQ-ArfGEF/BRAG1 is a novel component of retinal synaptic ribbons and forms a protein complex with RIBEYE.
  • [MeSH-major] Guanine Nucleotide Exchange Factors / metabolism. Nerve Tissue Proteins / metabolism. Retina / cytology. Synapses / metabolism. Synapses / ultrastructure

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19811534.001).
  • [ISSN] 1460-9568
  • [Journal-full-title] The European journal of neuroscience
  • [ISO-abbreviation] Eur. J. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Ctbp2 protein, mouse; 0 / DNA-Binding Proteins; 0 / Guanine Nucleotide Exchange Factors; 0 / IQSEC2 protein, mouse; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Nerve Tissue Proteins; 0 / Phosphoproteins; 0 / RNA, Messenger; EC 2.7.4.8 / Dlgh4 protein, mouse; EC 2.7.4.8 / Guanylate Kinase
  •  go-up   go-down


38. Rothermel A, Weigel W, Pfeiffer-Guglielmi B, Hamprecht B, Robitzki AA: Immunocytochemical analysis of glycogen phosphorylase isozymes in the developing and adult retina of the domestic chicken (Gallus domesticus). Neurochem Res; 2008 Feb;33(2):336-47
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunocytochemical analysis of glycogen phosphorylase isozymes in the developing and adult retina of the domestic chicken (Gallus domesticus).
  • Glycogen is the major energy reserve in neural tissues including the retina.
  • By applying isozyme-specific antibodies it could be demonstrated that the GP BB (brain), but not the GP MM (muscle) isoform is expressed in the chicken retina in neuronal and glial (Müller) cells.
  • In the embryonic chicken retina, GP showed a development-dependent expression pattern.
  • Double-labeling experiments with cell type-specific antibodies revealed that GP is expressed in various layers of the retina some of which, e.g., the photoreceptor inner segments, are known to be sites of high energy consumption.
  • [MeSH-major] Glycogen Phosphorylase / metabolism. Isoenzymes / metabolism. Retina / enzymology

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neurochem Res. 2006 Jan;31(1):103-8 [16475003.001]
  • [Cites] J Neurosci. 1998 Nov 1;18(21):8839-52 [9786990.001]
  • [Cites] Brain Res. 1983 Feb 14;261(1):138-44 [6301622.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1995 Jun;36(7):1259-70 [7775103.001]
  • [Cites] Eur J Neurosci. 1997 Sep;9(9):1795-803 [9383202.001]
  • [Cites] Mech Dev. 2000 Jun;94(1-2):25-36 [10842056.001]
  • [Cites] Acta Anat (Basel). 1988;132(3):256-9 [3414373.001]
  • [Cites] Histochemistry. 1993 Oct;100(4):265-70 [8276640.001]
  • [Cites] Invest Ophthalmol. 1973 Jun;12(6):434-48 [4541022.001]
  • [Cites] Glia. 2005 Jan 1;49(1):84-95 [15390095.001]
  • [Cites] Biochim Biophys Acta. 1986 Sep 12;878(2):159-67 [3756190.001]
  • [Cites] J Biol Chem. 1995 Jun 9;270(23):13748-56 [7775430.001]
  • [Cites] Science. 1991 May 17;252(5008):939-43 [2035024.001]
  • [Cites] J Comp Physiol A. 1991 Jul;169(1):39-50 [1941717.001]
  • [Cites] J Neurosci. 2005 Jun 1;25(22):5438-45 [15930394.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Sep 12;309(1):126-34 [12943673.001]
  • [Cites] J Neurosci Res. 2003 Oct 15;74(2):179-83 [14515346.001]
  • [Cites] J Neurosci. 2001 Feb 1;21(3):897-910 [11157076.001]
  • [Cites] Cell Tissue Res. 1996 Oct;286(1):13-22 [8781208.001]
  • [Cites] Clin Exp Ophthalmol. 2001 Jun;29(3):164-6 [11446460.001]
  • [Cites] J Neurocytol. 1992 Mar;21(3):171-83 [1532825.001]
  • [Cites] J Neurochem. 2004 May;89(3):537-52 [15086511.001]
  • [Cites] Dev Growth Differ. 1999 Dec;41(6):723-9 [10646802.001]
  • [Cites] J Neurochem. 1972 Dec;19(12):2759-66 [4652628.001]
  • [Cites] Brain Res Dev Brain Res. 1999 Dec 10;118(1-2):227-30 [10611524.001]
  • [Cites] Brain Res Rev. 2006 Aug 30;52(1):1-57 [16469387.001]
  • [Cites] Cell Mol Neurobiol. 2002 Feb;22(1):57-85 [12064518.001]
  • [Cites] Biomed Biochim Acta. 1983;42(10):1229-35 [6426476.001]
  • [Cites] Brain Res Rev. 2007 Jan;53(1):161-97 [17059846.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1997 Jun;38(7):1293-303 [9191592.001]
  • [Cites] Biochem Mol Biol Int. 1996 Sep;40(1):173-80 [8886283.001]
  • [Cites] J Physiol. 2003 Jun 1;549(Pt 2):501-12 [12679378.001]
  • [Cites] Ann N Y Acad Sci. 1986;478:220-32 [3541750.001]
  • [Cites] Exp Eye Res. 2006 Aug;83(2):235-46 [16690055.001]
  • [Cites] J Comp Neurol. 2006 Jun 1;496(4):544-55 [16572432.001]
  • [Cites] Brain Res. 1993 Oct 1;623(2):208-14 [8221102.001]
  • [Cites] Glia. 2006 Aug 15;54(3):214-22 [16819764.001]
  • [Cites] Prog Neurobiol. 2005 Jul;76(4):213-35 [16280194.001]
  • [Cites] Biochim Biophys Acta. 1992 Aug 21;1122(3):225-33 [1324005.001]
  • [Cites] Neuron. 2004 Dec 2;44(5):851-64 [15572115.001]
  • [Cites] Cell Tissue Res. 1997 May;288(2):267-78 [9082962.001]
  • [Cites] Neurochem Res. 1982 Oct;7(10):1307-17 [6218421.001]
  • [Cites] Prog Retin Eye Res. 2001 Mar;20(2):175-208 [11173251.001]
  • [Cites] Science. 1988 Oct 7;242(4875):90-1 [3175637.001]
  • [Cites] Cell Tissue Res. 1997 Jun;288(3):407-16 [9134854.001]
  • [Cites] J Neurophysiol. 2004 May;91(5):1999-2009 [14681336.001]
  • [Cites] Neurosci Lett. 2000 Sep 1;290(3):169-72 [10963890.001]
  • [Cites] Cell Calcium. 2005 May;37(5):425-32 [15820390.001]
  • [Cites] J Neurophysiol. 2004 May;91(5):1940 [15069092.001]
  • [Cites] J Neurosci Res. 1989 Mar;22(3):297-304 [2709446.001]
  • [Cites] Physiol Rev. 2005 Jul;85(3):883-941 [15987798.001]
  • [Cites] Histol Histopathol. 1998 Apr;13(2):531-52 [9589907.001]
  • [Cites] Brain Res. 2006 Sep 19;1110(1):23-9 [16879805.001]
  • [Cites] J Neurochem. 2003 Apr;85(1):73-81 [12641728.001]
  • [Cites] J Comp Neurol. 1992 Jun 8;320(2):257-66 [1377718.001]
  • [Cites] Development. 2002 May;129(9):2283-91 [11959835.001]
  • [Cites] Brain Res. 1995 Oct 2;694(1-2):128-32 [8974635.001]
  • [Cites] Neuron. 1999 Nov;24(3):673-85 [10595518.001]
  • [Cites] Nature. 2002 Jul 11;418(6894):177-81 [12110889.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Jun;47(6):2716-25 [16723491.001]
  • [Cites] Ann Anat. 1998 Aug;180(4):307-14 [9728270.001]
  • [Cites] Brain Res Mol Brain Res. 1989 Nov;6(2-3):177-85 [2615594.001]
  • [Cites] J Neurosci. 1997 Oct 15;17(20):7831-8 [9315903.001]
  • [Cites] Arch Ophthalmol. 1961 Nov;66:680-8 [14460992.001]
  • [Cites] J Neurosci. 1996 Feb 15;16(4):1430-9 [8778294.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 22;98(11):6417-22 [11344262.001]
  • [Cites] J Neurosci. 2000 Sep 15;20(18):6804-10 [10995824.001]
  • [Cites] Anal Biochem. 1976 May 7;72:248-54 [942051.001]
  • [Cites] J Neurosci Res. 2003 Apr 1;72(1):25-32 [12645076.001]
  • [Cites] J Bioenerg Biomembr. 1997 Aug;29(4):339-43 [9387094.001]
  • [Cites] Glia. 1994 Sep;12(1):62-7 [7843788.001]
  • [Cites] Eur J Neurosci. 2001 Mar;13(5):949-58 [11264667.001]
  • [Cites] J Neurosci. 1998 Jun 1;18(11):4155-65 [9592095.001]
  • [Cites] J Cereb Blood Flow Metab. 2002 Dec;22(12):1476-89 [12468892.001]
  • [Cites] Brain Res. 2007 Mar 9;1136(1):20-7 [17239832.001]
  • [Cites] J Ultrastruct Res. 1972 May;39(3):310-26 [4112747.001]
  • (PMID = 17940897.001).
  • [ISSN] 0364-3190
  • [Journal-full-title] Neurochemical research
  • [ISO-abbreviation] Neurochem. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Isoenzymes; EC 2.4.1.- / Glycogen Phosphorylase
  •  go-up   go-down


39. Zacks DN, Boehlke C, Richards AL, Zheng QD: Role of the Fas-signaling pathway in photoreceptor neuroprotection. Arch Ophthalmol; 2007 Oct;125(10):1389-95
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To determine whether inhibiting the Fas proapoptosis pathway will result in increased photoreceptor survival after separation of the retina from the retinal pigment epithelium (RPE).
  • METHODS: Retina/RPE separation was induced in rat and mouse eyes by the subretinal injection of hyaluronic acid, 1%.
  • Indices of photoreceptor death included terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) staining, cell counts, and retinal thickness measurements.
  • RESULTS: Inhibition of Fas signaling using Fas receptor-neutralizing antibody, siFas, or LPR mice resulted in a significant reduction in the number of TUNEL-positive photoreceptor cells as well as in a significant preservation of outer nuclear layer cell counts and thickness as compared with retina/RPE separation in eyes with intact Fas signaling.
  • CONCLUSIONS: Inhibition of the Fas proapoptosis pathway results in significant photoreceptor preservation after retinal separation from the RPE.
  • CLINICAL RELEVANCE: Fas-pathway inhibition might serve as a novel mechanism for preserving photoreceptor cells during retinal disease.
  • [MeSH-minor] Animals. Antibodies, Blocking / pharmacology. Apoptosis / drug effects. Cell Count. Cell Survival / physiology. Fluorescent Antibody Technique, Indirect. Immunoblotting. In Situ Nick-End Labeling. Mice. Mice, Inbred C57BL. Mice, Inbred MRL lpr. RNA / isolation & purification. RNA, Small Interfering / pharmacology. Rats. Rats, Inbred BN. Retinal Detachment / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Rhodopsin / metabolism. Rod Opsins / metabolism

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17923548.001).
  • [ISSN] 0003-9950
  • [Journal-full-title] Archives of ophthalmology (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch. Ophthalmol.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / K08-EY-14705
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Blocking; 0 / Antigens, CD95; 0 / Fas protein, mouse; 0 / RNA, Small Interfering; 0 / Rod Opsins; 0 / Tnfrsf6 protein, rat; 63231-63-0 / RNA; 9009-81-8 / Rhodopsin
  •  go-up   go-down


40. Kralj-Hans I, Tibber M, Jeffery G, Mobbs P: Differential effect of dopamine on mitosis in early postnatal albino and pigmented rat retinae. J Neurobiol; 2006 Jan;66(1):47-55
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Insufficient levels of L-DOPA, released from the retinal pigment epithelium (RPE), in albino animals are considered responsible for the abnormal development of the underlying neural retina.
  • L-DOPA normalizes retinal neurogenesis by reducing levels of cell proliferation either by acting on the cells directly or by being converted into dopamine.
  • Thus, the differential effects of dopamine on neural retinae from pigmented and albino rats in vitro must result from the activation of D1 receptors, which are present in the retina from birth.
  • These findings are discussed in light of previous reports of reduced catecholamine levels in the albino retina.
  • [MeSH-major] Dopamine / pharmacology. Mitosis / drug effects. Neurons / drug effects. Retina / cytology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOPAMINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16187306.001).
  • [ISSN] 0022-3034
  • [Journal-full-title] Journal of neurobiology
  • [ISO-abbreviation] J. Neurobiol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzazepines; 0 / Dopamine Antagonists; 0 / Receptors, Dopamine D1; EC 4.1.1.28 / Aromatic-L-Amino-Acid Decarboxylases; VTD58H1Z2X / Dopamine
  •  go-up   go-down


41. Nakamura H, Hayakawa K, Sawaguchi S, Gaja T: Removal of retinal indocyanine green dye by autologous serum irrigation in macular hole surgery. Retina; 2005 Sep;25(6):736-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Removal of retinal indocyanine green dye by autologous serum irrigation in macular hole surgery.
  • PURPOSE: To investigate the efficacy of autologous serum irrigation for removal of retinal indocyanine green (ICG) dye used to visualize the internal limiting membrane (ILM) in macular hole surgery.
  • Nine of 18 eyes underwent intravitreal autologous serum irrigation before completion of the surgery to remove residual ICG dye in the retina.
  • The main outcome measures were postoperative visual acuity, macular hole status, retinal pigment epithelial changes, and time course of ICG dye fading from the retina with or without intravitreal autologous serum irrigation.
  • ICG dye disappeared from the retina within an average of 6.1 months after surgery without serum and 2.4 months after surgery with serum (P < 0.01).
  • The application was simple and safe and significantly shortened the period of residual retinal ICG staining.
  • [MeSH-major] Coloring Agents / metabolism. Indocyanine Green / metabolism. Retina / metabolism. Retinal Perforations / surgery. Serum. Therapeutic Irrigation / methods

  • Hazardous Substances Data Bank. INDOCYANINE GREEN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16141861.001).
  • [ISSN] 0275-004X
  • [Journal-full-title] Retina (Philadelphia, Pa.)
  • [ISO-abbreviation] Retina (Philadelphia, Pa.)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coloring Agents; IX6J1063HV / Indocyanine Green
  •  go-up   go-down


42. Koinzer S, Elsner H, Klatt C, Pörksen E, Brinkmann R, Birngruber R, Roider J: Selective retina therapy (SRT) of chronic subfoveal fluid after surgery of rhegmatogenous retinal detachment: three case reports. Graefes Arch Clin Exp Ophthalmol; 2008 Oct;246(10):1373-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective retina therapy (SRT) of chronic subfoveal fluid after surgery of rhegmatogenous retinal detachment: three case reports.
  • BACKGROUND: Shallow subfoveal fluid accumulation after successful surgery for retinal detachment can be the reason for compromised visual acuity.
  • Selective retina therapy (SRT) is a new laser technology that uses a train of mus-laser pulses to selectively damage retinal pigment epithelial (RPE) cells while sparing retinal structures.
  • METHODS: We treated three patients with chronic subfoveal fluid accumulation after retinal detachment surgery.
  • The median period between retinal surgery and SRT treatment was 7 months.
  • In this situation where no other therapeutical options are established, SRT may be a beneficial treatment for chronic subfoveal fluid accumulation after retinal detachment surgery.
  • [MeSH-major] Body Fluids / metabolism. Lasers, Solid-State / therapeutic use. Low-Level Light Therapy / methods. Postoperative Complications. Retinal Detachment / surgery. Retinal Pigment Epithelium / surgery

  • MedlinePlus Health Information. consumer health - After Surgery.
  • MedlinePlus Health Information. consumer health - Retinal Detachment.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Ophthalmol. 2000 Jan;84(1):40-7 [10611098.001]
  • [Cites] Am J Ophthalmol. 2002 Apr;133(4):516-20 [11931785.001]
  • [Cites] Ophthalmology. 2006 Apr;113(4):666-72 [16581427.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 2002 Feb;240(2):85-9 [11931084.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 2004 Jul;242(7):576-81 [14997321.001]
  • [Cites] Am J Ophthalmol. 1987 Feb 15;103(2):167-79 [3492917.001]
  • [Cites] Lasers Surg Med. 2003;32(4):252-64 [12696092.001]
  • [Cites] Arch Ophthalmol. 1984 Mar;102(3):445-9 [6703994.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 2006 Dec;244(12):1638-45 [16758179.001]
  • [Cites] Lasers Surg Med. 2000;27(5):451-64 [11126439.001]
  • [Cites] J Biomed Opt. 2005 Nov-Dec;10(6):064022 [16409087.001]
  • [Cites] Semin Ophthalmol. 1999 Mar;14(1):19-26 [10790572.001]
  • [Cites] Ophthalmologe. 2006 Oct;103(10):856-60 [16937095.001]
  • [Cites] Am J Ophthalmol. 2000 Feb;129(2):186-90 [10682971.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8643-7 [8378341.001]
  • [Cites] Ophthalmologe. 1993 Jun;90(3):274-8 [8334331.001]
  • [Cites] Arch Ophthalmol. 1999 Aug;117(8):1028-34 [10448745.001]
  • [Cites] Eye (Lond). 2006 Nov;20(11):1284-7 [16200060.001]
  • [Cites] Ophthalmology. 2004 Jul;111(7):1340-3 [15234134.001]
  • [Cites] Arch Ophthalmol. 1992 Dec;110(12):1786-92 [1463423.001]
  • [Cites] Eye (Lond). 2007 Sep;21(9):1174-8 [16710430.001]
  • (PMID = 18546010.001).
  • [ISSN] 0721-832X
  • [Journal-full-title] Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie
  • [ISO-abbreviation] Graefes Arch. Clin. Exp. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  •  go-up   go-down


43. Lee EJ, Gibo TL, Grzywacz NM: Dark-rearing-induced reduction of GABA and GAD and prevention of the effect by BDNF in the mouse retina. Eur J Neurosci; 2006 Oct;24(8):2118-34
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dark-rearing-induced reduction of GABA and GAD and prevention of the effect by BDNF in the mouse retina.
  • Gamma-aminobutyric acid (GABA) is an important retinal neurotransmitter.
  • Second, can the retina recover from the effects of dark-rearing if returned to a normal light-dark cycle?
  • [MeSH-major] Brain-Derived Neurotrophic Factor / pharmacology. Glutamate Decarboxylase / biosynthesis. Isoenzymes / biosynthesis. Retina / drug effects. gamma-Aminobutyric Acid / biosynthesis

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. HEMATOXYLIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17074038.001).
  • [ISSN] 0953-816X
  • [Journal-full-title] The European journal of neuroscience
  • [ISO-abbreviation] Eur. J. Neurosci.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY08921; United States / NEI NIH HHS / EY / EY11170
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Brain-Derived Neurotrophic Factor; 0 / Coloring Agents; 0 / Isoenzymes; 56-12-2 / gamma-Aminobutyric Acid; EC 4.1.1.15 / Glutamate Decarboxylase; EC 4.1.1.15 / glutamate decarboxylase 2; YKM8PY2Z55 / Hematoxylin
  •  go-up   go-down


44. Kay JN, Link BA, Baier H: Staggered cell-intrinsic timing of ath5 expression underlies the wave of ganglion cell neurogenesis in the zebrafish retina. Development; 2005 Jun;132(11):2573-85
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Staggered cell-intrinsic timing of ath5 expression underlies the wave of ganglion cell neurogenesis in the zebrafish retina.
  • In the vertebrate retina, initiation of neurogenesis has recently been explained by a 'sequential-induction' model--signals from newly differentiated neurons are thought to trigger neurogenesis in adjacent progenitors, creating a wave of neurogenesis that spreads across the retina in a stereotypical manner.
  • We show here, however, that the wave of neurogenesis in the zebrafish retina can emerge through the independent action of progenitor cells--progenitors in different parts of the retina appear pre-specified to initiate neurogenesis at different times.
  • [MeSH-major] Cell Differentiation / physiology. DNA-Binding Proteins / metabolism. Ganglia, Sensory / embryology. Gene Expression Regulation, Developmental. Growth Substances / metabolism. Retinal Ganglion Cells / physiology. Zebrafish / embryology. Zebrafish Proteins / metabolism


45. Calamusa M, Pattabiraman PP, Pozdeyev N, Iuvone PM, Cellerino A, Domenici L: Specific alterations of tyrosine hydroxylase immunopositive cells in the retina of NT-4 knock out mice. Vision Res; 2007 May;47(11):1523-36
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Specific alterations of tyrosine hydroxylase immunopositive cells in the retina of NT-4 knock out mice.
  • To assess the effect of NT-4 deprivation on maturation of retinal circuitry, we investigated a mouse with targeted deletion of the gene encoding nt-4 (nt-4(-/-)).
  • In particular, we studied neurons immunostained by an antibody recognizing tyrosine hydroxylase (TH), the rate limiting enzyme for dopamine (DA) synthesis.
  • We found that TH immunopositive processes were altered in the retina of nt-4(-/-).
  • Alteration of TH immunopositive processes in nt-4(-/-) mice resulted in changes of DA turnover, as assessed by high-pressure liquid chromatography measurements.
  • These findings suggest that retinal NT-4 plays a role in the morphological maturation of dopaminergic retinal cells.

  • Hazardous Substances Data Bank. DOPAMINE .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17350071.001).
  • [ISSN] 0042-6989
  • [Journal-full-title] Vision research
  • [ISO-abbreviation] Vision Res.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / P30 EY006360; United States / NEI NIH HHS / EY / R01 EY004864; United States / NEI NIH HHS / EY / EY004864; United States / NEI NIH HHS / EY / EY014764
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Brain-Derived Neurotrophic Factor; 0 / Nerve Growth Factors; 0 / RNA, Messenger; 143551-63-7 / neurotrophin 4; EC 1.14.16.2 / Tyrosine 3-Monooxygenase; VTD58H1Z2X / Dopamine
  •  go-up   go-down


46. Cottaris NP, Elfar SD: How the retinal network reacts to epiretinal stimulation to form the prosthetic visual input to the cortex. J Neural Eng; 2005 Mar;2(1):S74-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How the retinal network reacts to epiretinal stimulation to form the prosthetic visual input to the cortex.
  • We considered the problem of determining how the retinal network may interact with electrical epiretinal stimulation in shaping the spike trains of ON and OFF ganglion cells, and thus the synaptic input to first-stage cortical neurons.
  • To do so, we developed a biophysical model of the retinal network with nine stacked neuronal mosaics.
  • Here, we describe the model's behavior under (i) electrical stimulation of a retina with complete cone photoreceptor loss, but an otherwise intact circuitry and (ii) electrical stimulation of a fully-functional retina.
  • Activation of the retinal network biases the excitation of ON relative to OFF ganglion cells, and in addition, gradually interpolates and focuses the initial, patchy synaptic input to the cortex.
  • These findings occur in both the normal and the degenerated retina simulations, but the normal retina exhibits a tighter spatiotemporal response.
  • [MeSH-minor] Animals. Computer Simulation. Humans. Photic Stimulation / methods. Prostheses and Implants. Retinal Degeneration / physiopathology. Retinal Ganglion Cells / physiology

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15876658.001).
  • [ISSN] 1741-2560
  • [Journal-full-title] Journal of neural engineering
  • [ISO-abbreviation] J Neural Eng
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] England
  •  go-up   go-down


47. Nakazawa T, Matsubara A, Noda K, Hisatomi T, She H, Skondra D, Miyahara S, Sobrin L, Thomas KL, Chen DF, Grosskreutz CL, Hafezi-Moghadam A, Miller JW: Characterization of cytokine responses to retinal detachment in rats. Mol Vis; 2006;12:867-78
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of cytokine responses to retinal detachment in rats.
  • PURPOSE: Photoreceptor apoptosis is associated with retinal detachment (RD) induced photoreceptor degeneration.
  • Retinal tissues were collected at various times (1, 3, 6, 24, and 72 h) after the induction of detachment.
  • To identify the cellular sources of the expressed genes, cells from various layers of the retina were obtained using laser capture microdissection (LCM), and their mRNAs were isolated.
  • RESULTS: At 72 h after RD a significant increase in mRNA levels for tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta), monocyte chemotactic protein-1 (MCP-1), and basic fibroblast growth factor (bFGF) were detected in the neural retina.
  • LCM revealed increased expression of mRNA for bFGF and MCP-1 in all retinal layers, though bFGF was especially evident in the outer nuclear layer (ONL) and MCP-1 in the inner nuclear layer (INL).
  • Immunohistochemistry showed TNF-alpha and bFGF expression in the whole retina, with IL-1beta specifically expressed in astrocytes and MCP-1 in Müller cells.
  • CONCLUSIONS: Retinal glial cells, including astrocytes and Müller cells, are a major source of cytokine induction after RD.
  • [MeSH-major] Chemokine CCL2 / metabolism. Fibroblast Growth Factor 2 / metabolism. Interleukin-1 / metabolism. Retinal Detachment / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Apoptosis. Astrocytes / metabolism. Enzyme-Linked Immunosorbent Assay. Immunohistochemistry. Male. Neuroglia / metabolism. Photoreceptor Cells, Vertebrate. RNA, Messenger / metabolism. Rats. Rats, Inbred BN. Retina / metabolism. Retina / pathology. Retinal Ganglion Cells / metabolism. Tissue Distribution

  • MedlinePlus Health Information. consumer health - Retinal Detachment.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16917487.001).
  • [ISSN] 1090-0535
  • [Journal-full-title] Molecular vision
  • [ISO-abbreviation] Mol. Vis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ccl2 protein, rat; 0 / Chemokine CCL2; 0 / Interleukin-1; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 103107-01-3 / Fibroblast Growth Factor 2
  •  go-up   go-down


48. Rajala RV: Phosphoinositide 3-kinase signaling in the vertebrate retina. J Lipid Res; 2010 Jan;51(1):4-22
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phosphoinositide 3-kinase signaling in the vertebrate retina.
  • Studies from our laboratory have shown that the retina and rod outer segments (ROSs) have active PI metabolism.
  • This article describes recent studies on the PI3K-generated PI lipid second messengers in the control and regulation of PI-binding proteins in the vertebrate retina.

  • MedlinePlus Health Information. consumer health - Diabetic Eye Problems.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Neurosci. 2000 Dec 1;20(23):8572-7 [11102460.001]
  • [Cites] Physiol Rev. 2001 Jan;81(1):117-151 [11152756.001]
  • [Cites] Curr Biol. 2001 Feb 20;11(4):213-21 [11250149.001]
  • [Cites] J Cell Biochem. 2001;81(3):523-34 [11255235.001]
  • [Cites] Biochemistry. 2001 Apr 17;40(15):4550-9 [11294622.001]
  • [Cites] FEBS Lett. 2001 Apr 13;494(3):225-31 [11311245.001]
  • [Cites] Biochim Biophys Acta. 2001 Oct 31;1533(3):190-206 [11731330.001]
  • [Cites] Nature. 2001 Dec 13;414(6865):799-806 [11742412.001]
  • [Cites] J Clin Invest. 2002 Jan;109(1):141-9 [11781359.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jan 8;99(1):419-24 [11752399.001]
  • [Cites] Mol Cell Biol. 2002 Feb;22(3):965-77 [11784871.001]
  • [Cites] Exp Eye Res. 2001 Oct;73(4):569-77 [11825027.001]
  • [Cites] Mol Cell Biol. 2002 Apr;22(8):2799-809 [11909972.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Apr 16;99(8):5313-8 [11959983.001]
  • [Cites] J Biol Chem. 2002 Jun 7;277(23):20336-42 [11916965.001]
  • [Cites] Dev Biol. 2002 Jul 15;247(2):295-306 [12086468.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Oct;43(10):3319-26 [12356841.001]
  • [Cites] J Biol Chem. 2002 Nov 8;277(45):43319-26 [12213821.001]
  • [Cites] FEBS Lett. 2003 Jan 16;534(1-3):164-8 [12527380.001]
  • [Cites] Prog Retin Eye Res. 2003 Jul;22(4):545-62 [12742394.001]
  • [Cites] Biochim Biophys Acta. 1980 Nov 7;620(2):212-26 [7002220.001]
  • [Cites] Biochim Biophys Acta. 1980 Nov 7;620(2):227-35 [6776991.001]
  • [Cites] Vision Res. 1980;20(12):1163-71 [7269272.001]
  • [Cites] J Biol Chem. 1983 Jun 10;258(11):6863-8 [6853507.001]
  • [Cites] J Neurochem. 1983 Jun;40(6):1630-8 [6854323.001]
  • [Cites] J Neurochem. 1983 Sep;41(3):764-71 [6308171.001]
  • [Cites] J Cell Biol. 1983 Sep;97(3):832-7 [6885920.001]
  • [Cites] Nature. 1983 Nov 3-9;306(5938):67-9 [6605482.001]
  • [Cites] J Cell Biol. 1984 Aug;99(2):686-91 [6086673.001]
  • [Cites] Biochem Biophys Res Commun. 1984 Aug 16;122(3):1397-403 [6236809.001]
  • [Cites] Cell. 2000 Oct 13;103(2):211-25 [11057895.001]
  • [Cites] Neuron. 2003 Jul 3;39(1):121-32 [12848937.001]
  • [Cites] EMBO J. 2003 Aug 15;22(16):4178-89 [12912916.001]
  • [Cites] Am J Physiol Endocrinol Metab. 2003 Oct;285(4):E763-74 [12799319.001]
  • [Cites] EMBO J. 2003 Oct 15;22(20):5501-10 [14532122.001]
  • [Cites] J Biol Chem. 2003 Nov 28;278(48):48453-66 [14504291.001]
  • [Cites] Mol Cell Biol. 2004 Jan;24(1):320-9 [14673165.001]
  • [Cites] J Neurochem. 2003 Dec;87(6):1427-35 [14713298.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Feb;45(2):675-84 [14744914.001]
  • [Cites] J Biol Chem. 2004 Mar 5;279(10):8986-90 [14699118.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):13086-94 [14711819.001]
  • [Cites] Diabetes. 2004 Apr;53(4):1162-5 [15047636.001]
  • [Cites] Biochemistry. 2004 May 18;43(19):5637-50 [15134438.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 2004 May;242(5):414-22 [14963717.001]
  • [Cites] Adv Exp Med Biol. 2003;533:369-76 [15180287.001]
  • [Cites] Exp Eye Res. 2004 Jul;79(1):51-9 [15183100.001]
  • [Cites] Mol Cell Biol. 2004 Oct;24(20):9137-51 [15456885.001]
  • [Cites] Science. 1971 Apr 2;172(3978):76-9 [5546288.001]
  • [Cites] Biochemistry. 1975 Apr 8;14(7):1343-52 [1079139.001]
  • [Cites] Science. 1976 Dec 3;194(4269):1071-4 [982063.001]
  • [Cites] Science. 1976 Dec 3;194(4269):1074-6 [1086510.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1979 Feb;18(2):117-32 [761968.001]
  • [Cites] J Biol Chem. 1997 Nov 28;272(48):30491-7 [9374542.001]
  • [Cites] Leuk Res. 1997 Sep;21(9):849-56 [9393600.001]
  • [Cites] J Biol Chem. 1997 Dec 12;272(50):31515-24 [9395488.001]
  • [Cites] Curr Biol. 1998 Jan 15;8(2):69-81 [9427642.001]
  • [Cites] Leuk Res. 1997 Nov-Dec;21(11-12):1027-31 [9444935.001]
  • [Cites] Science. 1998 Jan 30;279(5351):707-10 [9445476.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1432-7 [9465032.001]
  • [Cites] Science. 1998 May 1;280(5364):750-2 [9563954.001]
  • [Cites] J Biol Chem. 1998 May 8;273(19):11548-55 [9565570.001]
  • [Cites] Nature. 1984 Sep 13-19;311(5982):160-3 [6472474.001]
  • [Cites] Mol Cell Biochem. 1998 May;182(1-2):91-9 [9609118.001]
  • [Cites] Am J Physiol. 1984 Nov;247(5 Pt 2):H817-23 [6238541.001]
  • [Cites] Biochem Biophys Res Commun. 1984 Oct 30;124(2):503-6 [6093803.001]
  • [Cites] J Neurochem. 1985 Mar;44(3):773-8 [3919152.001]
  • [Cites] Biochem Biophys Res Commun. 1985 Apr 30;128(2):954-9 [2986631.001]
  • [Cites] J Cyclic Nucleotide Protein Phosphor Res. 1985;10(6):579-91 [3003171.001]
  • [Cites] Cell Struct Funct. 1986 Mar;11(1):53-63 [2420478.001]
  • [Cites] J Biol Chem. 1986 Apr 5;261(10):4749-57 [3007475.001]
  • [Cites] Science. 1986 Jul 18;233(4761):305-12 [3014651.001]
  • [Cites] Biochem Biophys Res Commun. 1987 Aug 14;146(3):1392-6 [3113434.001]
  • [Cites] Exp Eye Res. 1987 Jun;44(6):767-78 [3653272.001]
  • [Cites] Cell Struct Funct. 1987 Oct;12(5):471-81 [2824066.001]
  • [Cites] Exp Eye Res. 1987 Oct;45(4):545-56 [3428384.001]
  • [Cites] Nature. 1988 Apr 14;332(6165):644-6 [2833705.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2001 Dec;42(13):3110-7 [11726610.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2008 Apr;28(4):732-8 [18202321.001]
  • [Cites] J Neurosci. 2008 Mar 26;28(13):3456-67 [18367611.001]
  • [Cites] Neuroscience. 2008 Apr 22;153(1):214-25 [18358617.001]
  • [Cites] J Biol Chem. 2008 Jul 11;283(28):19781-92 [18480052.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 Aug;49(8):3687-98 [18421086.001]
  • [Cites] BMC Neurosci. 2008;9:78 [18691439.001]
  • [Cites] Exp Neurol. 2008 Oct;213(2):381-7 [18675804.001]
  • [Cites] Oncogene. 2008 Sep 18;27(41):5486-96 [18794883.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 Nov;49(11):4765-73 [18566464.001]
  • [Cites] Science. 2008 Nov 7;322(5903):963-6 [18988856.001]
  • [Cites] J Neurochem. 2008 Dec;107(5):1382-97 [18823366.001]
  • [Cites] J Biol Chem. 2008 Dec 5;283(49):34327-36 [18854316.001]
  • [Cites] Genes Dev. 2008 Nov 15;22(22):3147-57 [18997061.001]
  • [Cites] Nat Neurosci. 2009 Jan;12(1):44-52 [19060896.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2009 Feb;50(2):936-42 [18806289.001]
  • [Cites] Trends Genet. 2000 Oct;16(10):469-73 [11050335.001]
  • [Cites] Diabetes. 2001 Aug;50(8):1901-10 [11473054.001]
  • [Cites] Mol Vis. 2000 Nov 4;6:216-21 [11063755.001]
  • [Cites] J Neurochem. 2009 Mar;108(6):1607-20 [19166512.001]
  • [Cites] Diabetes. 2009 Jun;58(6):1356-64 [19252136.001]
  • [Cites] Biochemistry. 2009 Jun 23;48(24):5563-72 [19438210.001]
  • [Cites] J Neurochem. 2009 Sep;110(5):1648-60 [19575708.001]
  • [Cites] Cell Signal. 1999 Oct;11(10):719-25 [10574326.001]
  • [Cites] Exp Cell Res. 1999 Nov 25;253(1):239-54 [10579926.001]
  • [Cites] Genes Dev. 1999 Nov 15;13(22):2905-27 [10579998.001]
  • [Cites] J Biol Chem. 1999 Dec 10;274(50):35676-85 [10585447.001]
  • [Cites] Nat Cell Biol. 1999 Dec;1(8):500-6 [10587646.001]
  • [Cites] Eur J Neurosci. 1999 Dec;11(12):4349-56 [10594661.001]
  • [Cites] Genes Dev. 1999 Dec 15;13(24):3244-58 [10617573.001]
  • [Cites] Prog Retin Eye Res. 2000 Mar;19(2):205-21 [10674708.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1749-53 [10677529.001]
  • [Cites] J Biol Chem. 2000 Mar 17;275(11):7771-8 [10713090.001]
  • [Cites] J Neurosci. 2000 Apr 15;20(8):2792-9 [10751430.001]
  • [Cites] J Biol Chem. 2000 Apr 21;275(16):12069-73 [10766839.001]
  • [Cites] J Neurochem. 2000 Jul;75(1):355-62 [10854281.001]
  • [Cites] Mol Cell Biol. 2000 Aug;20(15):5479-89 [10891488.001]
  • [Cites] FEBS Lett. 2000 Jul 14;477(1-2):27-32 [10899305.001]
  • [Cites] Eur J Biochem. 2000 Aug;267(15):4705-12 [10903503.001]
  • [Cites] Diabetologia. 2000 Sep;43(9):1107-15 [11043856.001]
  • [Cites] Nat Methods. 2006 Apr;3(4):251-8 [16554828.001]
  • [Cites] Biochim Biophys Acta. 1988 Jun 30;970(2):205-11 [2838096.001]
  • [Cites] J Biol Chem. 1989 Apr 5;264(10):5996-6000 [2538432.001]
  • [Cites] Ann N Y Acad Sci. 1989;559:158-77 [2505653.001]
  • [Cites] J Biol Chem. 1989 Dec 5;264(34):20181-4 [2555343.001]
  • [Cites] Biochemistry. 1990 Jun 12;29(23):5442-6 [2167126.001]
  • [Cites] Exp Eye Res. 1990 Aug;51(2):167-76 [2167231.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7365-9 [1699226.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8550-4 [2236064.001]
  • [Cites] Nature. 2001 Jan 4;409(6816):92-7 [11343120.001]
  • [Cites] Mol Cell Biol. 2005 Nov;25(21):9491-502 [16227599.001]
  • [Cites] J Biol Chem. 2001 Aug 31;276(35):32814-21 [11443130.001]
  • [Cites] Mol Endocrinol. 2001 Oct;15(10):1768-80 [11579209.001]
  • [Cites] Curr Biol. 2001 Oct 16;11(20):1636-42 [11676927.001]
  • [Cites] Microvasc Res. 2001 Nov;62(3):252-62 [11678628.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jul 1;90(13):6042-6 [8327481.001]
  • [Cites] J Biol Chem. 1993 Aug 25;268(24):18181-6 [8349693.001]
  • [Cites] Curr Eye Res. 1993 Aug;12(8):727-32 [8222733.001]
  • [Cites] J Biol Chem. 1993 Dec 5;268(34):25455-62 [8244979.001]
  • [Cites] Mol Cell Biol. 1993 Dec;13(12):7677-88 [8246984.001]
  • [Cites] J Biol Chem. 1994 Jan 7;269(1):1-4 [8276779.001]
  • [Cites] J Biol Chem. 1994 Jan 7;269(1):29-32 [8276809.001]
  • [Cites] J Biol Chem. 1994 Apr 1;269(13):9850-6 [8144577.001]
  • [Cites] J Biol Chem. 1994 Apr 8;269(14):10217-20 [8144601.001]
  • [Cites] Cell. 1994 Apr 8;77(1):83-93 [8156600.001]
  • [Cites] EMBO J. 1994 Apr 1;13(7):1557-65 [8156994.001]
  • [Cites] Nature. 1995 Mar 2;374(6517):60-1 [7870171.001]
  • [Cites] J Biol Chem. 1995 Mar 24;270(12):6710-7 [7896814.001]
  • [Cites] Biochem Soc Trans. 1995 Feb;23(1):76-80 [7758794.001]
  • [Cites] J Biol Chem. 1995 Jun 2;270(22):13271-6 [7768926.001]
  • [Cites] J Clin Invest. 1995 Jun;95(6):2806-12 [7769120.001]
  • [Cites] Biochemistry. 1995 Jun 13;34(23):7722-7 [7779819.001]
  • [Cites] J Biol Chem. 1995 Jun 16;270(24):14376-82 [7540168.001]
  • [Cites] Mol Cell Biol. 1995 Aug;15(8):4453-65 [7542745.001]
  • [Cites] J Biol Chem. 1995 Sep 1;270(35):20503-8 [7544790.001]
  • [Cites] Metabolism. 1995 Sep;44(9):1175-84 [7666792.001]
  • [Cites] Nature. 1995 Oct 5;377(6548):441-6 [7566123.001]
  • [Cites] Curr Eye Res. 1995 Nov;14(11):1025-9 [8585931.001]
  • [Cites] Mol Cell Biol. 1996 May;16(5):2195-203 [8628286.001]
  • [Cites] J Biol Chem. 1996 Mar 8;271(10):5317-20 [8621382.001]
  • [Cites] Curr Eye Res. 2003 Jan;26(1):55-63 [12789537.001]
  • [Cites] J Clin Invest. 2003 Jun;111(12):1835-42 [12813019.001]
  • [Cites] FEBS Lett. 2003 Jul 3;546(1):140-8 [12829250.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Jun 9;344(3):912-9 [16631611.001]
  • [Cites] Cell Metab. 2006 May;3(5):355-66 [16679293.001]
  • [Cites] Nature. 2006 May 18;441(7091):366-70 [16625210.001]
  • [Cites] Cell. 2006 May 19;125(4):733-47 [16647110.001]
  • [Cites] Nat Rev Genet. 2006 Aug;7(8):606-19 [16847462.001]
  • [Cites] Eur J Neurosci. 2006 Aug;24(4):981-90 [16930425.001]
  • [Cites] Can J Physiol Pharmacol. 2006 Jul;84(7):667-75 [16998530.001]
  • [Cites] J Biol Chem. 1996 May 24;271(21):12502-10 [8647858.001]
  • [Cites] Biochem J. 1996 Jul 1;317 ( Pt 1):291-5 [8694778.001]
  • [Cites] J Biol Chem. 1996 Aug 16;271(33):19810-6 [8702689.001]
  • [Cites] Diabetes. 1996 Oct;45(10):1379-85 [8826975.001]
  • [Cites] Mol Cell Biol. 1996 Nov;16(11):6242-51 [8887654.001]
  • [Cites] Cytokine Growth Factor Rev. 1996 Aug;7(2):153-9 [8899293.001]
  • [Cites] EMBO J. 1996 Dec 2;15(23):6541-51 [8978681.001]
  • [Cites] J Neurosci. 1997 Mar 1;17(5):1548-60 [9030615.001]
  • [Cites] Cell. 1997 Feb 21;88(4):435-7 [9038334.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1995-2000 [9050893.001]
  • [Cites] Cell. 1997 Apr 4;89(1):105-14 [9094719.001]
  • [Cites] J Biol Chem. 1997 Apr 18;272(16):10341-4 [9099669.001]
  • [Cites] Neurochem Res. 1997 Apr;22(4):373-8 [9130246.001]
  • [Cites] J Neurochem. 1997 Jul;69(1):53-9 [9202293.001]
  • [Cites] J Clin Invest. 1997 Jul 15;100(2):449-58 [9218523.001]
  • [Cites] Neurochem Res. 1997 Aug;22(8):951-6 [9239750.001]
  • [Cites] Trends Biochem Sci. 1997 Jul;22(7):267-72 [9255069.001]
  • [Cites] J Biol Chem. 1997 Aug 22;272(34):21520-6 [9261171.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1997 Aug;38(9):1873-82 [9286278.001]
  • [Cites] Proc Soc Exp Biol Med. 1997 Oct;216(1):1-20 [9316606.001]
  • [Cites] Metabolism. 1997 Oct;46(10):1140-5 [9322796.001]
  • [Cites] J Neurochem. 1997 Oct;69(4):1693-702 [9326298.001]
  • [Cites] Adv Second Messenger Phosphoprotein Res. 1997;31:263-77 [9344257.001]
  • [Cites] Science. 1997 Nov 14;278(5341):1319-22 [9360933.001]
  • [Cites] J Biol Chem. 1998 May 29;273(22):13375-8 [9593664.001]
  • [Cites] Mol Cell Biochem. 1998 May;182(1-2):101-8 [9609119.001]
  • [Cites] Exp Eye Res. 1998 Jun;66(6):817-21 [9657914.001]
  • [Cites] J Biol Chem. 1998 Oct 2;273(40):26026-35 [9748281.001]
  • [Cites] Annu Rev Biochem. 1998;67:481-507 [9759495.001]
  • [Cites] J Biol Chem. 1998 Oct 9;273(41):26908-14 [9756938.001]
  • [Cites] Biochem J. 1998 Oct 15;335 ( Pt 2):417-24 [9761742.001]
  • [Cites] J Biol Chem. 1998 Nov 6;273(45):29600-6 [9792669.001]
  • [Cites] Biochim Biophys Acta. 1998 Dec 8;1436(1-2):151-64 [9838087.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14950-5 [9843996.001]
  • [Cites] Mol Cell. 1998 Dec;2(6):887-93 [9885576.001]
  • [Cites] Science. 1999 Jan 15;283(5400):390-2 [9888854.001]
  • [Cites] Science. 1999 Jan 15;283(5400):393-7 [9888855.001]
  • [Cites] Annu Rev Cell Dev Biol. 1998;14:231-64 [9891784.001]
  • [Cites] Biochem J. 1999 Feb 1;337 ( Pt 3):575-83 [9895304.001]
  • [Cites] Nat Genet. 1999 Feb;21(2):230-5 [9988280.001]
  • [Cites] Mol Cell Biol. 1999 Mar;19(3):2278-88 [10022914.001]
  • [Cites] Science. 1999 Mar 5;283(5407):1544-8 [10066179.001]
  • [Cites] Mol Cell Biol. 1999 Apr;19(4):2921-8 [10082559.001]
  • [Cites] J Biol Chem. 1999 Mar 26;274(13):8347-50 [10085060.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Feb 5;255(1):169-74 [10082674.001]
  • [Cites] J Biol Chem. 1999 Apr 16;274(16):10669-72 [10196133.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4633-8 [10200314.001]
  • [Cites] Trends Cell Biol. 1999 Apr;9(4):125-8 [10203785.001]
  • [Cites] Curr Opin Cell Biol. 1999 Apr;11(2):177-83 [10209148.001]
  • [Cites] Chem Biol. 1999 May;6(5):R129-36 [10322127.001]
  • [Cites] Mol Cell Biol. 1999 Jun;19(6):4525-34 [10330191.001]
  • [Cites] Pharmacol Ther. 1999 May-Jun;82(2-3):409-25 [10454216.001]
  • [Cites] J Biol Chem. 1999 Oct 15;274(42):30236-43 [10514516.001]
  • [Cites] J Biol Chem. 1999 Oct 22;274(43):30896-905 [10521483.001]
  • [Cites] J Biol Chem. 2009 Feb 6;284(6):3521-8 [19068483.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2009 Mar;50(3):1033-40 [19029027.001]
  • [Cites] Vitam Horm. 2009;80:583-612 [19251051.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Oct;47(10):4598-606 [17003457.001]
  • [Cites] Biochem Soc Trans. 2006 Nov;34(Pt 5):647-62 [17052169.001]
  • [Cites] Trends Cell Biol. 2006 Nov;16(11):560-8 [16996267.001]
  • [Cites] J Neurosci. 2007 Jan 3;27(1):203-11 [17202487.001]
  • [Cites] Adv Exp Med Biol. 2006;572:491-7 [17249614.001]
  • [Cites] Cell Signal. 2007 May;19(5):1081-92 [17275257.001]
  • [Cites] J Biol Chem. 2007 Mar 30;282(13):9865-73 [17272282.001]
  • [Cites] Mol Cell. 2007 Mar 23;25(6):917-31 [17386267.001]
  • [Cites] Mol Cell Biol. 2007 Apr;27(8):2830-40 [17283057.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 8;104(19):7809-14 [17470792.001]
  • [Cites] Eur J Hum Genet. 2007 Jun;15(6):664-71 [17377520.001]
  • [Cites] Cell. 2007 Jun 29;129(7):1261-74 [17604717.001]
  • [Cites] J Endocrinol. 2007 Aug;194(2):243-56 [17641274.001]
  • [Cites] Cell. 2007 Aug 10;130(3):535-47 [17693260.001]
  • [Cites] J Biol Chem. 2007 Oct 5;282(40):29584-93 [17635910.001]
  • [Cites] FEBS J. 2007 Dec;274(23):6025-36 [17949438.001]
  • [Cites] Cell Signal. 2008 Jan;20(1):21-30 [17716864.001]
  • [Cites] Biochemistry. 1999 Oct 19;38(42):13787-94 [10529223.001]
  • [Cites] J Biol Chem. 1960 Jun;235:PC23-4 [13828720.001]
  • [Cites] Diabetologia. 2004 Oct;47(10):1735-46 [15502926.001]
  • [Cites] Curr Eye Res. 2004 Oct-Nov;29(4-5):349-55 [15590482.001]
  • [Cites] J Cell Sci. 2004 Dec 15;117(Pt 26):6497-509 [15572406.001]
  • [Cites] Prog Retin Eye Res. 2005 Mar;24(2):275-306 [15610977.001]
  • [Cites] J Neurosci. 2005 Feb 2;25(5):1240-8 [15689562.001]
  • [Cites] J Biol Chem. 2005 Feb 11;280(6):5121-7 [15611065.001]
  • [Cites] Mol Cell Biol. 2005 Mar;25(5):1596-607 [15713620.001]
  • [Cites] Curr Biol. 2005 Mar 29;15(6):566-70 [15797027.001]
  • [Cites] Cell Tissue Res. 2005 May;320(2):213-22 [15789220.001]
  • [Cites] J Cell Sci. 2005 May 1;118(Pt 9):2005-12 [15840652.001]
  • [Cites] Biochemistry. 2005 Jun 7;44(22):7929-35 [15924411.001]
  • [Cites] Biol Cell. 2005 Jul;97(7):501-18 [15966865.001]
  • [Cites] Mol Cell Neurosci. 2005 Aug;29(4):569-79 [15936213.001]
  • [Cites] J Cell Biol. 2005 Aug 1;170(3):455-64 [16043515.001]
  • [Cites] Biochemistry. 2005 Nov 29;44(47):15461-71 [16300394.001]
  • [Cites] J Biol Chem. 2005 Dec 9;280(49):40406-16 [16221682.001]
  • [Cites] J Cell Sci. 2005 Dec 15;118(Pt 24):5675-8 [16339964.001]
  • [Cites] Curr Biol. 2006 Jan 24;16(2):140-9 [16431366.001]
  • [Cites] J Cell Sci. 2006 Feb 15;119(Pt 4):605-14 [16467569.001]
  • [Cites] Thromb Haemost. 2006 Jan;95(1):29-35 [16543958.001]
  • [Cites] Biochem Soc Trans. 2006 Apr;34(Pt 2):213-6 [16545079.001]
  • [Cites] J Biol Chem. 1990 Nov 15;265(32):19704-11 [2174051.001]
  • [Cites] Transplant Proc. 1991 Apr;23(2 Suppl 2):1-5 [1712132.001]
  • [Cites] Mol Cell Biol. 1991 Nov;11(11):5541-50 [1922062.001]
  • [Cites] Trends Biochem Sci. 1991 Aug;16(8):297-301 [1659758.001]
  • [Cites] Biochemistry. 1991 Nov 26;30(47):11302-6 [1659898.001]
  • [Cites] Cell. 1992 Feb 7;68(3):545-60 [1739967.001]
  • [Cites] Mol Cell Biol. 1992 Apr;12(4):1451-9 [1312663.001]
  • [Cites] Diabetes Care. 1992 Mar;15(3):318-68 [1532777.001]
  • [Cites] J Cell Biol. 1992 Apr;117(2):401-14 [1373143.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 May 1;89(9):4052-6 [1570332.001]
  • [Cites] Nature. 1992 Jul 2;358(6381):70-3 [1614535.001]
  • [Cites] Cell. 1992 Jun 26;69(7):1227-36 [1377606.001]
  • [Cites] J Biol Chem. 1992 Jun 25;267(18):12393-6 [1319994.001]
  • [Cites] J Biol Chem. 1992 Jul 15;267(20):13811-4 [1321126.001]
  • [Cites] Nature. 1992 Jul 16;358(6383):239-42 [1321346.001]
  • [Cites] J Neurosci Res. 1992 Mar;31(3):584-90 [1640507.001]
  • [Cites] Cell. 1992 Aug 7;70(3):419-29 [1322797.001]
  • [Cites] Science. 1992 Aug 14;257(5072):973-7 [1380182.001]
  • [Cites] EMBO J. 1992 Sep;11(9):3469-79 [1380456.001]
  • [Cites] Nature. 1993 Jan 28;361(6410):315-25 [8381210.001]
  • [Cites] Brain Res. 1993 Feb 26;604(1-2):142-8 [8384508.001]
  • [Cites] J Biol Chem. 1993 Jun 5;268(16):11479-81 [8505282.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Apr;47(4):1620-9 [16565401.001]
  • [Cites] Diabetes. 2006 Apr;55(4):1148-56 [16567541.001]
  • (PMID = 19638643.001).
  • [ISSN] 1539-7262
  • [Journal-full-title] Journal of lipid research
  • [ISO-abbreviation] J. Lipid Res.
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P20 RR017703; United States / NEI NIH HHS / EY / P30 EY012190; United States / NEI NIH HHS / EY / EY12190; United States / NEI NIH HHS / EY / R01 EY000871; United States / NCRR NIH HHS / RR / P20-RR17703; United States / NEI NIH HHS / EY / EY016507; United States / NEI NIH HHS / EY / EY00871; United States / NEI NIH HHS / EY / R01 EY016507
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Phosphatidylinositols; 0 / Protein Subunits; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.1.3.48 / Protein Tyrosine Phosphatases
  • [Number-of-references] 291
  • [Other-IDs] NLM/ PMC2789784
  •  go-up   go-down


49. Kram YA, Mantey S, Corbo JC: Avian cone photoreceptors tile the retina as five independent, self-organizing mosaics. PLoS One; 2010 Feb 01;5(2):e8992
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Avian cone photoreceptors tile the retina as five independent, self-organizing mosaics.
  • The avian retina possesses one of the most sophisticated cone photoreceptor systems among vertebrates.
  • Here we show that the five cone types of the chicken independently tile the retina as highly ordered mosaics with a characteristic spacing between cones of the same type.
  • Since regular photoreceptor spacing is critical for uniform sampling of visual space, the cone mosaics of the avian retina represent an elegant example of the emergence of adaptive global patterning secondary to simple local interactions between individual photoreceptors.
  • Our results indicate that the evolutionary pressures that gave rise to the avian retina's various adaptations for enhanced color discrimination also acted to fine-tune its spatial sampling of color and luminance.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Comp Neurol. 2001 Mar 19;431(4):363-81 [11223808.001]
  • [Cites] Prog Retin Eye Res. 2000 Nov;19(6):711-77 [11029553.001]
  • [Cites] Phys Rev Lett. 2002 Apr 1;88(13):138302 [11955131.001]
  • [Cites] Curr Biol. 2002 Apr 16;12(8):657-60 [11967153.001]
  • [Cites] J Theor Biol. 2002 Apr 7;215(3):345-61 [12054842.001]
  • [Cites] J Theor Biol. 2003 Mar 21;221(2):289-300 [12628235.001]
  • [Cites] J Comp Neurol. 2003 Jun 16;461(1):123-36 [12722109.001]
  • [Cites] Proc Biol Sci. 2003 Jun 22;270(1521):1255-61 [12816638.001]
  • [Cites] Nat Rev Neurosci. 2004 Oct;5(10):747-57 [15378035.001]
  • [Cites] J Ultrastruct Res. 1966 Dec;16(5):672-84 [5954546.001]
  • [Cites] J Comp Neurol. 1970 Nov;140(3):359-98 [5476889.001]
  • [Cites] Exp Eye Res. 1973 Nov 25;17(4):347-55 [4765257.001]
  • [Cites] Vis Neurosci. 1991 Feb;6(2):95-111 [2049333.001]
  • [Cites] J Comp Neurol. 1992 Apr 22;318(4):355-66 [1578007.001]
  • [Cites] Vis Neurosci. 1992 Aug;9(2):169-80 [1504026.001]
  • [Cites] J Comp Neurol. 1995 Sep 4;359(4):537-50 [7499546.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 23;93(2):577-81 [8570598.001]
  • [Cites] Vis Neurosci. 1996 Jan-Feb;13(1):15-30 [8730986.001]
  • [Cites] J Comp Neurol. 1996 Jul 22;371(2):222-34 [8835728.001]
  • [Cites] Vis Neurosci. 1997 Sep-Oct;14(5):811-26 [9364720.001]
  • [Cites] Rev Bras Biol. 1996 Dec;56 Su 1 Pt 2:199-207 [9394501.001]
  • [Cites] Proc Biol Sci. 1998 Mar 7;265(1394):351-8 [9523436.001]
  • [Cites] Eur J Neurosci. 1999 Apr;11(4):1461-9 [10103140.001]
  • [Cites] J Theor Biol. 1999 Sep 21;200(2):231-44 [10504288.001]
  • [Cites] Int J Dev Biol. 2004;48(8-9):935-45 [15558484.001]
  • [Cites] J Neurosci Res. 2005 Feb 1;79(3):401-11 [15605374.001]
  • [Cites] Dev Biol. 2005 Feb 15;278(2):381-95 [15680358.001]
  • [Cites] J Comp Physiol A Neuroethol Sens Neural Behav Physiol. 2005 Apr;191(4):381-92 [15711964.001]
  • [Cites] Proc Biol Sci. 2005 Sep 7;272(1574):1745-52 [16096084.001]
  • [Cites] Development. 2005 Oct;132(19):4353-62 [16141228.001]
  • [Cites] J Neurosci. 2005 Oct 19;25(42):9669-79 [16237171.001]
  • [Cites] Math Med Biol. 2006 Jun;23(2):79-99 [16510463.001]
  • [Cites] Nature. 2006 Aug 31;442(7106):1038-41 [16900102.001]
  • [Cites] Int Rev Cytol. 2007;259:173-224 [17425942.001]
  • [Cites] Vis Neurosci. 2008 Mar-Apr;25(2):209-14 [18334045.001]
  • [Cites] J Neurosci. 2009 Jan 7;29(1):106-17 [19129389.001]
  • [Cites] Dev Biol. 2009 Feb 1;326(1):86-100 [19013445.001]
  • [Cites] Vis Neurosci. 2009 Jan-Feb;26(1):5-19 [19193250.001]
  • [Cites] PLoS Comput Biol. 2009 Jun;5(6):e1000412 [19521504.001]
  • [Cites] Philos Trans R Soc Lond B Biol Sci. 2009 Oct 12;364(1531):2925-40 [19720654.001]
  • [Cites] Philos Trans R Soc Lond B Biol Sci. 2009 Oct 12;364(1531):2941-55 [19720655.001]
  • [Cites] Vision Res. 1982;22(9):1205-10 [7147731.001]
  • [Cites] Vision Res. 1977;17(7):755-64 [898682.001]
  • [Cites] Biol Cybern. 1977 Oct 14;27(4):229-33 [588625.001]
  • [Cites] Proc R Soc Lond B Biol Sci. 1978 Mar 22;200(1141):441-61 [26058.001]
  • [Cites] Science. 1983 Jul 22;221(4608):382-5 [6867716.001]
  • [Cites] Vision Res. 1984;24(2):129-37 [6710875.001]
  • [Cites] J Comp Neurol. 1984 Mar 20;224(1):107-15 [6715574.001]
  • [Cites] Vision Res. 1985;25(1):145-7 [3984213.001]
  • [Cites] Vision Res. 1984;24(11):1661-71 [6533991.001]
  • [Cites] Trends Neurosci. 2000 Jan;23(1):26-34 [10631786.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Feb 29;97(5):2303-7 [10688875.001]
  • [Cites] Eur J Neurosci. 2000 Feb;12(2):613-20 [10712641.001]
  • [Cites] J Comp Physiol A. 2001 Nov;187(9):685-97 [11778831.001]
  • (PMID = 20126550.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01 EY018826; United States / NEI NIH HHS / EY / R01EY018826; United States / Howard Hughes Medical Institute / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oils; 0 / Retinal Pigments
  • [Other-IDs] NLM/ PMC2813877
  •  go-up   go-down


50. Tucker BA, Redenti SM, Jiang C, Swift JS, Klassen HJ, Smith ME, Wnek GE, Young MJ: The use of progenitor cell/biodegradable MMP2-PLGA polymer constructs to enhance cellular integration and retinal repopulation. Biomaterials; 2010 Jan;31(1):9-19
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The use of progenitor cell/biodegradable MMP2-PLGA polymer constructs to enhance cellular integration and retinal repopulation.
  • The inability of the adult mammalian retina to regenerate can be partly attributed to the expression of injury-induced inhibitory extracellular matrix (ECM) and cell adhesion molecules.
  • In particular, photoreceptor degeneration stimulates deposition of the inhibitory ECM proteins neurocan and CD44 at the outer limits of the dystrophic retina, where they act as a barrier against cellular migration and axonal extension.
  • We have previously shown that degradation of these molecules, via induction of MMP2, promotes host-donor integration and retinal repopulation following transplantation.
  • Here we present a biodegradable/biocompatible polymer scaffold that has the ability to deliver MMP2, in conjunction with retinal progenitor cells, directly to the site of retinal injury in an attempt to enhance cellular integration and promote retinal repopulation.
  • Following delivery, significant degradation of CD44 and neurocan from the outer limits of the dystrophic retina, without further disruption of retinal architecture, was observed.
  • As a result, the number of retinal progenitor cells that migrated beyond the glial barrier into the degenerating host increased significantly.
  • These cells took up residence in the retinal outer nuclear layer, adopted appropriate photoreceptor morphology and expressed the mature photoreceptor markers recoverin and rhodopsin.
  • Thus, we have created a cell delivery platform that upon transplantation provides controlled release of active-MMP2 directly to the site of retinal injury, stimulating inhibitory ECM barrier removal and enhancement of stem cell integration and retinal repopulation.
  • [MeSH-major] Lactic Acid / metabolism. Matrix Metalloproteinase 2 / metabolism. Polyglycolic Acid / metabolism. Retina / metabolism. Stem Cells / cytology

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. LACTIC ACID .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19775744.001).
  • [ISSN] 1878-5905
  • [Journal-full-title] Biomaterials
  • [ISO-abbreviation] Biomaterials
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / polylactic acid-polyglycolic acid copolymer; 26009-03-0 / Polyglycolic Acid; 33X04XA5AT / Lactic Acid; EC 3.4.24.24 / Matrix Metalloproteinase 2
  •  go-up   go-down


51. Garcia-Frigola C, Carreres MI, Vegar C, Herrera E: Gene delivery into mouse retinal ganglion cells by in utero electroporation. BMC Dev Biol; 2007;7:103
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene delivery into mouse retinal ganglion cells by in utero electroporation.
  • BACKGROUND: The neural retina is a highly structured tissue of the central nervous system that is formed by seven different cell types that are arranged in layers.
  • Despite much effort, the genetic mechanisms that underlie retinal development are still poorly understood.
  • In recent years, large-scale genomic analyses have identified candidate genes that may play a role in retinal neurogenesis, axon guidance and other key processes during the development of the visual system.
  • Gene delivery techniques have been described to express exogenous proteins in the retina of newborn mice but these approaches do not efficiently introduce genes into the only retinal cell type that transmits visual information to the brain, the retinal ganglion cells (RGCs).
  • [MeSH-major] Gene Expression Regulation, Developmental. Gene Transfer Techniques. Retinal Ganglion Cells

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Neurosci. 2003 Dec;6(12):1277-83 [14625554.001]
  • [Cites] J Comp Neurol. 1979 Nov 15;188(2):263-72 [500859.001]
  • [Cites] Neuron. 2000 Dec;28(3):779-92 [11163266.001]
  • [Cites] Nat Rev Neurosci. 2001 Feb;2(2):109-18 [11252990.001]
  • [Cites] Nat Rev Genet. 2000 Oct;1(1):20-9 [11262869.001]
  • [Cites] Neuroscience. 2001;103(4):865-72 [11301197.001]
  • [Cites] Micron. 2002;33(1):1-6 [11473808.001]
  • [Cites] Nat Neurosci. 2001 Nov;4 Suppl:1156-8 [11687822.001]
  • [Cites] Dev Biol. 2001 Dec 1;240(1):237-46 [11784059.001]
  • [Cites] Neuron. 2003 Sep 11;39(6):919-35 [12971893.001]
  • [Cites] Cell. 2003 Sep 5;114(5):545-57 [13678579.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jan 6;101(1):16-22 [14603031.001]
  • [Cites] Development. 2004 Aug;131(15):3773-84 [15240555.001]
  • [Cites] PLoS Biol. 2004 Sep;2(9):E247 [15226823.001]
  • [Cites] J Neurosci. 1988 Apr;8(4):1194-205 [3357016.001]
  • [Cites] Vis Neurosci. 1993 Jan-Feb;10(1):117-30 [8424921.001]
  • [Cites] J Neurobiol. 1993 Oct;24(10):1400-22 [8228964.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 23;93(2):589-95 [8570600.001]
  • [Cites] Cell. 2004 Nov 12;119(4):567-78 [15537545.001]
  • [Cites] J Neurosci Methods. 2005 Apr 30;143(2):151-8 [15814147.001]
  • [Cites] J Neurosci. 2005 Apr 20;25(16):4014-23 [15843603.001]
  • [Cites] Gene Ther. 2005 May;12(10):843-51 [15789063.001]
  • [Cites] Nat Neurosci. 2005 Aug;8(8):1022-7 [16025107.001]
  • [Cites] Nat Neurosci. 2005 Aug;8(8):1013-21 [16025110.001]
  • [Cites] Development. 2004 Nov;131(22):5727-39 [15509772.001]
  • [Cites] Cell. 2000 Jul 7;102(1):77-88 [10929715.001]
  • (PMID = 17875204.001).
  • [ISSN] 1471-213X
  • [Journal-full-title] BMC developmental biology
  • [ISO-abbreviation] BMC Dev. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2080638
  •  go-up   go-down


52. Hauck SM, Kinkl N, Deeg CA, Swiatek-de Lange M, Schöffmann S, Ueffing M: GDNF family ligands trigger indirect neuroprotective signaling in retinal glial cells. Mol Cell Biol; 2006 Apr;26(7):2746-57
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GDNF family ligands trigger indirect neuroprotective signaling in retinal glial cells.
  • Apoptotic cell death of photoreceptors is the final event leading to blindness in the heterogeneous group of inherited retinal degenerations.
  • GDNF (glial cell-line-derived neurotrophic factor) was found to rescue photoreceptor function and survival very effectively in an animal model of retinal degeneration (M.
  • We show here that in porcine retina, GDNF receptors GFRalpha-1 and RET are expressed on retinal Mueller glial cells (RMG) but not on photoreceptors.
  • We correlate the findings to intact porcine retina, where GDNF induces phosphorylation of ERK in the perinuclear region of RMG located in the inner nuclear layer.
  • We provide here a detailed model of GDNF-induced signaling in mammalian retina and propose that the GDNF-induced rescue effect on mutated photoreceptors is an indirect effect mediated by retinal Mueller glial cells.
  • [MeSH-major] Glial Cell Line-Derived Neurotrophic Factor / metabolism. Neuroglia / metabolism. Neuroprotective Agents / metabolism. Retina / cytology. Signal Transduction

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neuron. 2000 May;26(2):533-41 [10839371.001]
  • [Cites] J Neurobiol. 1999 Feb 15;38(3):382-90 [10022580.001]
  • [Cites] Dev Immunol. 2000;7(2-4):89-101 [11097204.001]
  • [Cites] Biochem J. 2000 Oct 1;351(Pt 1):95-105 [10998351.001]
  • [Cites] J Neurosci. 2001 Mar 1;21(5):1464-72 [11222636.001]
  • [Cites] Mol Ther. 2001 May;3(5 Pt 1):746-56 [11356079.001]
  • [Cites] Am J Pathol. 2001 Sep;159(3):1113-20 [11549604.001]
  • [Cites] Front Biosci. 2001 Oct 1;6:E72-92 [11578954.001]
  • [Cites] J Biol Chem. 2001 Nov 23;276(47):43871-8 [11571286.001]
  • [Cites] Exp Eye Res. 2001 Nov;73(5):693-701 [11747369.001]
  • [Cites] Neuropharmacology. 2002 Jan;42(1):9-19 [11750912.001]
  • [Cites] Neuroscience. 2002;110(3):555-67 [11906793.001]
  • [Cites] Nat Rev Neurosci. 2002 May;3(5):383-94 [11988777.001]
  • [Cites] Exp Eye Res. 2002 Apr;74(4):435-44 [12076087.001]
  • [Cites] Exp Eye Res. 2002 Jun;74(6):703-17 [12126944.001]
  • [Cites] J Cell Biochem. 2003 Jan 1;88(1):57-75 [12461775.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Jan;44(1):355-64 [12506096.001]
  • [Cites] Cell. 2003 Jun 27;113(7):867-79 [12837245.001]
  • [Cites] Dev Ophthalmol. 2003;37:109-25 [12876833.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Oct;44(10):4550-8 [14507904.001]
  • [Cites] Neuroscience. 2003;122(1):229-35 [14596863.001]
  • [Cites] Glia. 2003 Dec;44(3):251-63 [14603466.001]
  • [Cites] Cancer Lett. 2004 Feb 20;204(2):197-211 [15013219.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Apr;45(4):1240-6 [15037593.001]
  • [Cites] Exp Eye Res. 1981 Jun;32(6):755-69 [7250225.001]
  • [Cites] Comput Biol Med. 1984;14(4):437-45 [6548944.001]
  • [Cites] Vet Clin North Am Large Anim Pract. 1984 Nov;6(3):667-76 [6440337.001]
  • [Cites] Exp Eye Res. 1988 Dec;47(6):839-53 [2905672.001]
  • [Cites] Exp Eye Res. 1990 May;50(5):475-82 [2373151.001]
  • [Cites] Nature. 1990 Sep 6;347(6288):83-6 [2168521.001]
  • [Cites] J Neurocytol. 1990 Aug;19(4):550-65 [2243247.001]
  • [Cites] Cell. 1991 Feb 22;64(4):841-8 [1847668.001]
  • [Cites] J Anat. 1991 Oct;178:65-77 [1810936.001]
  • [Cites] Science. 1993 May 21;260(5111):1130-2 [8493557.001]
  • [Cites] J Biol Chem. 1994 Feb 18;269(7):5241-8 [8106507.001]
  • [Cites] Brain Res Mol Brain Res. 1994 Dec;27(2):310-4 [7898315.001]
  • [Cites] J Neurosci Res. 1995 Sep 1;42(1):131-43 [8531222.001]
  • [Cites] Cancer Metastasis Rev. 1996 Jun;15(2):177-86 [8842489.001]
  • [Cites] Cell Tissue Res. 1996 Nov;286(2):191-207 [8854888.001]
  • [Cites] Cell Tissue Res. 1996 Dec;286(3):325-36 [8929335.001]
  • [Cites] J Pathol. 1997 Jun;182(2):233-7 [9274536.001]
  • [Cites] Eur J Neurosci. 1999 Apr;11(4):1202-16 [10103116.001]
  • [Cites] Mol Cell Neurosci. 1999 May;13(5):313-25 [10356294.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1999 Oct;40(11):2724-34 [10509671.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Jan;46(1):367-74 [15623797.001]
  • [Cites] Mol Vis. 2005;11:232-44 [15827545.001]
  • [Cites] FEBS Lett. 1999 Nov 12;461(1-2):120-4 [10561508.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Mar;41(3):927-36 [10711715.001]
  • [Cites] Neuron. 2000 May;26(2):285-6 [10839346.001]
  • [Cites] Ann Neurol. 1994 Feb;35(2):151-63 [8109896.001]
  • [Cites] Biochem J. 1997 Oct 1;327 ( Pt 1):1-16 [9355727.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1998 Mar;39(3):592-602 [9501871.001]
  • [Cites] Vision Res. 1998 May;38(10):1505-15 [9667015.001]
  • [Cites] J Neurosci. 1998 Dec 1;18(23):9662-72 [9822727.001]
  • [Cites] Bioorg Med Chem Lett. 1998 Oct 20;8(20):2839-44 [9873633.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Oct;41(11):3622-33 [11006261.001]
  • (PMID = 16537917.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glial Cell Line-Derived Neurotrophic Factor; 0 / Glial Cell Line-Derived Neurotrophic Factor Receptors; 0 / Ligands; 0 / Nerve Tissue Proteins; 0 / Neural Cell Adhesion Molecules; 0 / Neuroprotective Agents; 0 / Neurturin; 0 / RNA, Messenger; 103107-01-3 / Fibroblast Growth Factor 2; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
  • [Other-IDs] NLM/ PMC1430306
  •  go-up   go-down


53. Conte I, Carrella S, Avellino R, Karali M, Marco-Ferreres R, Bovolenta P, Banfi S: miR-204 is required for lens and retinal development via Meis2 targeting. Proc Natl Acad Sci U S A; 2010 Aug 31;107(35):15491-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] miR-204 is required for lens and retinal development via Meis2 targeting.
  • Morpholino-mediated ablation of miR-204 expression resulted in an eye phenotype characterized by microphthalmia, abnormal lens formation, and altered dorsoventral (D-V) patterning of the retina, which is associated with optic fissure coloboma.
  • These data provide an example of how a specific miRNA can regulate multiple events in eye formation; at the same time, they uncover an as yet unreported function of Meis2 in the specification of D-V patterning of the retina.
  • [MeSH-major] Fish Proteins / genetics. Lens, Crystalline / metabolism. MicroRNAs / genetics. Retina / metabolism. Transcription Factors / genetics

  • SciCrunch. OMIM: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Development. 2008 May;135(10):1735-43 [18403413.001]
  • [Cites] Development. 2005 Sep;132(18):4131-42 [16107473.001]
  • [Cites] Nat Rev Genet. 2004 Jul;5(7):522-31 [15211354.001]
  • [Cites] Biochim Biophys Acta. 2008 Aug;1779(8):471-8 [18194678.001]
  • [Cites] Curr Opin Genet Dev. 2005 Aug;15(4):410-5 [15979303.001]
  • [Cites] Pathogenetics. 2009 Nov 04;2(1):7 [19889204.001]
  • [Cites] PLoS Biol. 2007 Aug;5(8):e203 [17676975.001]
  • [Cites] J Neurosci. 2008 May 7;28(19):4878-87 [18463241.001]
  • [Cites] Int J Biochem Cell Biol. 2007;39(10):1754-9 [17707680.001]
  • [Cites] Dev Biol. 2007 May 1;305(1):1-13 [17335797.001]
  • [Cites] Science. 2007 Oct 12;318(5848):271-4 [17761850.001]
  • [Cites] J Biol Chem. 2009 Sep 18;284(38):25791-803 [19608742.001]
  • [Cites] Mech Dev. 2009 Oct;126(10):804-16 [19703558.001]
  • [Cites] Mech Dev. 2004 Jul;121(7-8):605-18 [15210170.001]
  • [Cites] J Biol Chem. 2007 Aug 24;282(34):25053-66 [17597072.001]
  • [Cites] Prog Retin Eye Res. 2009 Mar;28(2):87-116 [19071227.001]
  • [Cites] J Biol Chem. 2004 Nov 5;279(45):47272-7 [15322073.001]
  • [Cites] Genes Dev. 2006 May 1;20(9):1187-202 [16651659.001]
  • [Cites] Development. 1997 Aug;124(16):3147-56 [9272955.001]
  • [Cites] Genome Biol. 2007;8(7):R137 [17617896.001]
  • [Cites] Annu Rev Cell Dev Biol. 2001;17:255-96 [11687490.001]
  • [Cites] Nature. 2004 Feb 19;427(6976):745-9 [14973488.001]
  • [Cites] Nat Rev Neurosci. 2001 May;2(5):333-42 [11331917.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2007 Feb;48(2):509-15 [17251443.001]
  • [Cites] Development. 2000 Oct;127(20):4325-34 [11003833.001]
  • [Cites] Nat Rev Neurosci. 2001 Feb;2(2):109-18 [11252990.001]
  • [Cites] Development. 2008 Mar;135(5):805-11 [18216174.001]
  • [Cites] Trends Biochem Sci. 2007 Apr;32(4):189-97 [17350266.001]
  • [Cites] Mamm Genome. 2008 Aug;19(7-8):510-6 [18648874.001]
  • [Cites] Cell. 1996 Jul 12;86(1):71-82 [8689689.001]
  • [Cites] Cancer Res. 2008 Oct 15;68(20):8499-506 [18922924.001]
  • [Cites] PLoS Comput Biol. 2010 Apr;6(4):e1000730 [20369013.001]
  • [Cites] Genes Dev. 2002 Aug 15;16(16):2097-107 [12183364.001]
  • [Cites] Nat Genet. 2007 Feb;39(2):259-63 [17220889.001]
  • [Cites] J Biol Chem. 1998 Nov 27;273(48):32265-72 [9822705.001]
  • [Cites] Genome Res. 2009 Mar;19(3):481-90 [19088304.001]
  • [Cites] Development. 2008 Mar;135(5):799-803 [18216175.001]
  • [Cites] Nat Rev Mol Cell Biol. 2009 Feb;10(2):141-8 [19145236.001]
  • [Cites] EMBO J. 2006 May 17;25(10):2107-18 [16675956.001]
  • [Cites] Genes Dev. 2009 May 1;23(9):1046-51 [19372388.001]
  • [Cites] Int J Dev Biol. 2004;48(8-9):783-91 [15558471.001]
  • (PMID = 20713703.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] Italy / Telethon / / TGM06D01
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fish Proteins; 0 / Homeodomain Proteins; 0 / MicroRNAs; 0 / Transcription Factors
  • [Other-IDs] NLM/ PMC2932609
  •  go-up   go-down


54. Hogewind BF, Mukhopadhyay A, Theelen T, Hollander AI, Hoyng CB: Variable clinical spectrum of the myocilin Gln368X mutation in a Dutch family with primary open angle glaucoma. Curr Eye Res; 2010 Jan;35(1):31-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • She and her six siblings were examined clinically, including Heidelberg Retina Tomography II, and venous blood samples were screened for other variants in MYOC, WDR36, OPTN, and CYP1B1.
  • Two of these four siblings had glaucomatous optic disc changes with corresponding visual field losses and abnormal Heidelberg Retina Tomography results by the Moorfields regression analysis, one had abnormal results by the Moorfields regression analysis but no visual field loss, and one showed no glaucomatous signs or symptoms at all.

  • Genetic Alliance. consumer health - Glaucoma.
  • Genetic Alliance. consumer health - Primary open angle glaucoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [ErratumIn] Curr Eye Res. 2010 Apr;35(4):361
  • (PMID = 20021252.001).
  • [ISSN] 1460-2202
  • [Journal-full-title] Current eye research
  • [ISO-abbreviation] Curr. Eye Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / Eye Proteins; 0 / Glycoproteins; 0 / trabecular meshwork-induced glucocorticoid response protein
  •  go-up   go-down


55. Kiser PD, Golczak M, Lodowski DT, Chance MR, Palczewski K: Crystal structure of native RPE65, the retinoid isomerase of the visual cycle. Proc Natl Acad Sci U S A; 2009 Oct 13;106(41):17325-30
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Vertebrate vision is maintained by the retinoid (visual) cycle, a complex enzymatic pathway that operates in the retina to regenerate the visual chromophore, 11-cis-retinal.
  • This enzyme catalyzes the conversion of all-trans-retinyl esters to 11-cis-retinol in the retinal pigment epithelium (RPE).

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. IRON, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Biol Chem. 2000 Apr 21;275(16):11915-20 [10766819.001]
  • [Cites] FEBS J. 2009 Jun;276(11):3020-30 [19490105.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Aug;41(9):2735-42 [10937591.001]
  • [Cites] Biochemistry. 2000 Sep 19;39(37):11370-80 [10985782.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Dec;41(13):4293-9 [11095629.001]
  • [Cites] J Biol Chem. 2001 Mar 2;276(9):6560-5 [11092891.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2001 Jun;42(7):1429-35 [11381042.001]
  • [Cites] Genomics. 2001 Mar 1;72(2):193-202 [11401432.001]
  • [Cites] Hum Mutat. 2001 Aug;18(2):164 [11462243.001]
  • [Cites] Biochemistry. 2003 Feb 25;42(7):2229-38 [12590612.001]
  • [Cites] Hum Mutat. 2004 Apr;23(4):306-17 [15024725.001]
  • [Cites] Cell. 2004 Jun 11;117(6):761-71 [15186777.001]
  • [Cites] Biochemistry. 1986 Oct 21;25(21):6473-8 [3491624.001]
  • [Cites] Biochemistry. 1988 May 31;27(11):4147-52 [3261995.001]
  • [Cites] Science. 1989 May 26;244(4907):968-71 [2727688.001]
  • [Cites] J Biol Chem. 1993 Jul 25;268(21):15751-7 [8340400.001]
  • [Cites] Science. 1997 Jun 20;276(5320):1872-4 [9188535.001]
  • [Cites] Nat Genet. 1997 Oct;17(2):139-41 [9326927.001]
  • [Cites] Nat Genet. 1997 Oct;17(2):194-7 [9326941.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 17;95(6):3088-93 [9501220.001]
  • [Cites] Proteins. 2005 May 1;59(2):252-65 [15723347.001]
  • [Cites] Science. 2005 Apr 8;308(5719):267-9 [15821095.001]
  • [Cites] Cell. 2005 Aug 12;122(3):449-59 [16096063.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 30;102(35):12413-8 [16116091.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13658-63 [16150724.001]
  • [Cites] FEBS Lett. 2005 Oct 10;579(24):5414-8 [16198348.001]
  • [Cites] Mol Vis. 2005;11:1151-65 [16379027.001]
  • [Cites] J Biol Chem. 2006 Feb 3;281(5):2835-40 [16319067.001]
  • [Cites] Annu Rev Biochem. 2006;75:743-67 [16756510.001]
  • [Cites] J Biol Chem. 2006 Aug 4;281(31):21820-6 [16754667.001]
  • [Cites] Biochemistry. 2006 Sep 5;45(35):10710-8 [16939223.001]
  • [Cites] Cell Mol Life Sci. 2006 Oct;63(19-20):2291-303 [16909205.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Dec;47(12):5191-6 [17122102.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2007;47:469-512 [16968212.001]
  • [Cites] J Biol Chem. 2007 Jul 20;282(29):20915-24 [17504753.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2007 Sep;48(9):4284-90 [17724218.001]
  • [Cites] J Mol Biol. 2007 Sep 21;372(3):774-97 [17681537.001]
  • [Cites] Chemistry. 2008;14(7):2264-76 [18181127.001]
  • [Cites] Science. 2008 Jul 11;321(5886):213-6 [18621661.001]
  • [Cites] Biochemistry. 2008 Sep 16;47(37):9856-65 [18722466.001]
  • [Cites] Bioinformatics. 2008 Dec 1;24(23):2780-1 [18818215.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):19000-5 [19020100.001]
  • [Cites] J Biol Chem. 2009 Jan 30;284(5):3211-8 [19049981.001]
  • (PMID = 19805034.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01 EY009339; United States / NIGMS NIH HHS / GM / U54-GM074945; United States / NEI NIH HHS / EY / T32 EY007157; United States / NEI NIH HHS / EY / L40 EY017820; United States / NIGMS NIH HHS / GM / U54 GM074945; United States / NEI NIH HHS / EY / EY009339-20S1; United States / NIBIB NIH HHS / EB / P03-EB09998; United States / NEI NIH HHS / EY / R01 EY009339-20S1; United States / NEI NIH HHS / EY / R01-EY009339; United States / NIBIB NIH HHS / EB / P30 EB009998
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Eye Proteins; 36-88-4 / Carotenoids; E1UOL152H7 / Iron
  • [Other-IDs] NLM/ PMC2765077
  •  go-up   go-down


56. Pham H, Yu H, Laski FA: Cofilin/ADF is required for retinal elongation and morphogenesis of the Drosophila rhabdomere. Dev Biol; 2008 Jun 1;318(1):82-91
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cofilin/ADF is required for retinal elongation and morphogenesis of the Drosophila rhabdomere.
  • These changes include a five-fold elongation of the retinal cell body and the morphogenesis of the rhabdomere, the light sensing structure of the cell.
  • In tsr mutants, the retina is shorter than normal, the result of a lack of retinal elongation.
  • We propose, and provide data supporting, that these wide rhabdomeres and adherens junctions are secondary events caused by the inhibition of retinal elongation.

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • FlyBase. FlyBase .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Cell Biol. 1995 Dec;131(5):1243-59 [8522587.001]
  • [Cites] Dev Biol. 1995 Oct;171(2):415-33 [7556924.001]
  • [Cites] Nature. 2002 Mar 14;416(6877):143-9 [11850625.001]
  • [Cites] Cell. 2003 Feb 21;112(4):453-65 [12600310.001]
  • [Cites] Dev Biol. 1976 Oct 15;53(2):217-40 [825400.001]
  • [Cites] Cell. 1985 Apr;40(4):767-74 [3886158.001]
  • [Cites] Cell. 1988 Aug 26;54(5):659-64 [3044607.001]
  • [Cites] Dev Biol. 1989 Dec;136(2):346-62 [2511048.001]
  • [Cites] Genes Dev. 1991 Apr;5(4):583-93 [2010085.001]
  • [Cites] Genes Dev. 1991 Jun;5(6):970-83 [2044963.001]
  • [Cites] Development. 1991 Nov;113(3):841-50 [1726564.001]
  • [Cites] Development. 1993 Apr;117(4):1223-37 [8404527.001]
  • [Cites] Development. 1993 Nov;119(3):855-65 [8187644.001]
  • [Cites] J Mol Biol. 1997 Jun 20;269(4):459-67 [9217250.001]
  • [Cites] J Cell Biol. 1997 Aug 25;138(4):771-81 [9265645.001]
  • [Cites] Curr Opin Cell Biol. 1998 Feb;10(1):45-51 [9484594.001]
  • [Cites] Nature. 1998 Jun 25;393(6687):805-9 [9655397.001]
  • [Cites] Nature. 1998 Jun 25;393(6687):809-12 [9655398.001]
  • [Cites] Curr Biol. 1999 Mar 11;9(5):R160-3 [10074445.001]
  • [Cites] J Cell Sci. 1999 May;112 ( Pt 10):1553-65 [10212149.001]
  • [Cites] Trends Cell Biol. 1999 Sep;9(9):364-70 [10461190.001]
  • [Cites] Nature. 1999 Oct 7;401(6753):542-3 [10524617.001]
  • [Cites] PLoS Biol. 2005 Feb;3(2):e59 [15719063.001]
  • [Cites] Annu Rev Biomed Eng. 2005;7:187-221 [16004570.001]
  • [Cites] Mech Dev. 2005 Nov;122(11):1194-205 [16169194.001]
  • [Cites] Trends Cell Biol. 2007 Jan;17(1):26-35 [17134901.001]
  • [Cites] Nat Rev Cancer. 2007 Jun;7(6):429-40 [17522712.001]
  • [Cites] Genetics. 2007 Aug;176(4):2223-34 [17565945.001]
  • [Cites] J Biol Chem. 1999 Nov 12;274(46):32531-4 [10551802.001]
  • [Cites] Nature. 2000 Apr 27;404(6781):1007-11 [10801131.001]
  • [Cites] Annu Rev Biophys Biomol Struct. 2000;29:545-76 [10940259.001]
  • [Cites] Nat Cell Biol. 2001 Feb;3(2):204-9 [11175754.001]
  • [Cites] Science. 2001 May 25;292(5521):1502-6 [11379633.001]
  • [Cites] Cell. 2002 Jan 25;108(2):233-46 [11832213.001]
  • [Cites] Nature. 2002 Mar 14;416(6877):178-83 [11850624.001]
  • [Cites] EMBO J. 1995 Mar 15;14(6):1209-20 [7720711.001]
  • [Cites] Development. 1995 Dec;121(12):4359-70 [8575336.001]
  • (PMID = 18423434.001).
  • [ISSN] 1095-564X
  • [Journal-full-title] Developmental biology
  • [ISO-abbreviation] Dev. Biol.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY014876-04; United States / NEI NIH HHS / EY / R01 EY014876-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actin Depolymerizing Factors; 0 / Drosophila Proteins; 0 / Microfilament Proteins; 0 / twinstar protein, Drosophila
  • [Other-IDs] NLM/ NIHMS53180; NLM/ PMC2713181
  •  go-up   go-down


57. Bakri SJ, Pulido JS, Mukherjee P, Marler RJ, Mukhopadhyay D: Absence of histologic retinal toxicity of intravitreal nanogold in a rabbit model. Retina; 2008 Jan;28(1):147-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Absence of histologic retinal toxicity of intravitreal nanogold in a rabbit model.
  • PURPOSE: To evaluate the retinal toxicity of intravitreal nanogold, a novel antiangiogenic and long-term delivery agent.
  • The retina and retinal pigment epithelium were otherwise histologically normal.
  • CONCLUSION: Intravitreal nanogold at concentrations of 67 micromol/0.1 mL and 670 micromol/0.1 mL showed no signs of retinal or optic nerve toxicity by light microscopy during histologic examination at 1 month.
  • [MeSH-major] Gold / toxicity. Metal Nanoparticles / toxicity. Retina / drug effects

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GOLD, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18185152.001).
  • [ISSN] 0275-004X
  • [Journal-full-title] Retina (Philadelphia, Pa.)
  • [ISO-abbreviation] Retina (Philadelphia, Pa.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 7440-57-5 / Gold
  •  go-up   go-down


58. Beleboni RO, Guizzo R, Fontana AC, Pizzo AB, Carolino RO, Gobbo-Neto L, Lopes NP, Coutinho-Netto J, Dos Santos WF: Neurochemical characterization of a neuroprotective compound from Parawixia bistriata spider venom that inhibits synaptosomal uptake of GABA and glycine. Mol Pharmacol; 2006 Jun;69(6):1998-2006
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • According to our experimental glaucoma data in rat retina, FrPbAII is able to cross the blood-retina barrier and promote effective protection of retinal layers submitted to ischemic conditions.
  • [MeSH-minor] Animals. Biological Transport / drug effects. GABA Plasma Membrane Transport Proteins / drug effects. GABA-B Receptor Agonists. Glaucoma / prevention & control. Glycine Plasma Membrane Transport Proteins / drug effects. Ion Channels / antagonists & inhibitors. Male. Rats. Rats, Inbred BB. Retina / drug effects. Spiders / metabolism

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GLYCINE .
  • Hazardous Substances Data Bank. UREA .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16551783.001).
  • [ISSN] 0026-895X
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-amino-5-ureidopentanamide; 0 / GABA Plasma Membrane Transport Proteins; 0 / GABA-B Receptor Agonists; 0 / Glycine Plasma Membrane Transport Proteins; 0 / Ion Channels; 0 / Neuroprotective Agents; 0 / Spider Venoms; 56-12-2 / gamma-Aminobutyric Acid; 8W8T17847W / Urea; TE7660XO1C / Glycine
  •  go-up   go-down


59. Pojda-Wilczek D, Herba E, Pojda SM: [Flash full-field electroretinography in diseases with night blindness]. Klin Oczna; 2005;107(1-3):28-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: The aim of this study is to present similarities and differences of electroretinograms in early stages of retinal diseases with nyctalopia.
  • RESULTS: In diseases with nyctalopia the function of peripheral retina is markedly abnormal and scotopic ERG is significantly reduced or even absent.
  • Well preserved a-wave distinguished ERG of patients with stationary night blindness from the other progressive diseases of retina or choroid.
  • CONCLUSIONS: In patients with nyctalopia using ERG is possible to obtain which retinal elements do not work but it is only start point to following diagnostic examinations, to make proper final diagnosis.
  • [MeSH-major] Electroretinography. Night Blindness / diagnosis. Retinal Diseases / complications

  • Genetic Alliance. consumer health - Blindness.
  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16052794.001).
  • [ISSN] 0023-2157
  • [Journal-full-title] Klinika oczna
  • [ISO-abbreviation] Klin Oczna
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  •  go-up   go-down


60. Rhee KD, Yang XJ: Function and mechanism of CNTF/LIF signaling in retinogenesis. Adv Exp Med Biol; 2010;664:647-54
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ciliary neurotrophic factor (CNTF) and leukemia inhibitory factor (LIF) exhibit multiple biological effects in the developing vertebrate retina.
  • Moreover, LIF also inhibits retinal vascular development.
  • CNTF/LIF signaling components CNTFRalpha, LIFRbeta, gp130, and a number of STAT proteins are expressed in the retina.
  • CNTF/LIF activates Jak-STAT, ERK, and Notch pathways during retinal development.
  • Perturbation of CNTF induced signal transduction reveals that different combinations of CNTF/LIF signaling pathways regulate differentiation of retinal neurons and glia.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell Mol Life Sci. 2000 Feb;57(2):224-34 [10766019.001]
  • [Cites] Stem Cells. 2008 Oct;26(10):2611-24 [18669911.001]
  • [Cites] Neuron. 2000 May;26(2):383-94 [10839357.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Dec;41(13):4317-23 [11095633.001]
  • [Cites] J Neurosci. 2001 Feb 15;21(4):1265-73 [11160397.001]
  • [Cites] Nat Rev Neurosci. 2001 Feb;2(2):109-18 [11252990.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Sep;43(9):3099-108 [12202535.001]
  • [Cites] Gene Expr Patterns. 2003 Mar;3(1):109-13 [12609612.001]
  • [Cites] Exp Eye Res. 2003 Apr;76(4):421-31 [12634107.001]
  • [Cites] Mol Vis. 2003 Dec 16;9:715-22 [14685141.001]
  • [Cites] Semin Cell Dev Biol. 2004 Feb;15(1):91-103 [15036212.001]
  • [Cites] Mol Vis. 2004 Jun 3;10:366-75 [15205663.001]
  • [Cites] Mol Cell Neurosci. 2004 Jun;26(2):258-70 [15207851.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Jul;45(7):2407-12 [15223824.001]
  • [Cites] Mol Cell Neurosci. 2004 Sep;27(1):32-43 [15345241.001]
  • [Cites] Science. 1988 Mar 4;239(4844):1142-5 [2449732.001]
  • [Cites] Neuron. 1990 Jun;4(6):833-45 [2163263.001]
  • [Cites] Science. 1993 Dec 3;262(5139):1575-9 [7504325.001]
  • [Cites] J Biol Chem. 1994 Apr 15;269(15):11648-55 [7512571.001]
  • [Cites] Neurosci Lett. 1994 Oct 24;180(2):163-6 [7700572.001]
  • [Cites] Development. 1995 Aug;121(8):2695-706 [7671829.001]
  • [Cites] J Neurosci. 1996 Oct 1;16(19):6089-99 [8815891.001]
  • [Cites] J Neurochem. 1997 Mar;68(3):979-90 [9048743.001]
  • [Cites] Development. 1997 Mar;124(5):1055-67 [9056780.001]
  • [Cites] Development. 1997 Jun;124(12):2345-54 [9199361.001]
  • [Cites] Cell. 1997 Nov 14;91(4):531-41 [9390562.001]
  • [Cites] Cell Tissue Res. 1998 Feb;291(2):207-16 [9426308.001]
  • [Cites] J Biol Chem. 1998 Apr 17;273(16):9703-10 [9545305.001]
  • [Cites] J Neurosci. 1998 May 15;18(10):3620-9 [9570793.001]
  • [Cites] Ann N Y Acad Sci. 1998 May 1;840:97-106 [9629241.001]
  • [Cites] J Neurosci. 2004 Nov 3;24(44):9779-88 [15525763.001]
  • [Cites] Stem Cells. 2005 Mar;23(3):424-32 [15749937.001]
  • [Cites] Mol Vis. 2005;11:232-44 [15827545.001]
  • [Cites] Dev Neurosci. 2004;26(5-6):359-70 [15855765.001]
  • [Cites] Mol Vis. 2005;11:298-308 [15889014.001]
  • [Cites] Exp Eye Res. 2005 Jul;81(1):103-15 [15978261.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Jul;46(7):2601-10 [15980254.001]
  • [Cites] J Neurosci Res. 2005 Nov 1;82(3):316-32 [16206277.001]
  • [Cites] Dev Biol. 2006 Oct 15;298(2):527-39 [16914133.001]
  • [Cites] Dev Biol. 2006 Dec 15;300(2):583-98 [17054938.001]
  • [Cites] Mol Vis. 2007;13:206-19 [17327826.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jul 3;104(27):11292-7 [17592117.001]
  • [Cites] Mol Cell Biol. 2007 Dec;27(23):8318-29 [17908793.001]
  • [Cites] Cell Tissue Res. 2008 Oct;334(1):7-16 [18665395.001]
  • [Cites] Development. 2000 Jun;127(12):2515-22 [10821751.001]
  • (PMID = 20238069.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY012270-08; United States / NEI NIH HHS / EY / R01 EY012270; United States / NEI NIH HHS / EY / R01 EY019052; United States / NEI NIH HHS / EY / R01 EY012270-08
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ciliary Neurotrophic Factor; 0 / Leukemia Inhibitory Factor
  • [Other-IDs] NLM/ NIHMS201371; NLM/ PMC3234160
  •  go-up   go-down


61. Mochida H, Sato K, Momose-Sato Y: Switching of the transmitters that mediate hindbrain correlated activity in the chick embryo. Eur J Neurosci; 2009 Jan;29(1):14-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In some structures, such as the retina and spinal cord, it has been shown that the dominant transmitter mediating the correlated wave switches from acetylcholine to glutamate during development, although the functional significance of this phenomenon has not been clarified.
  • The results show for the first time that the dominant transmitter switches from acetylcholine to glutamate in a region other than the retina and spinal cord.

  • Hazardous Substances Data Bank. GLUTAMIC ACID HYDROCHLORIDE .
  • Hazardous Substances Data Bank. STRYCHNINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19087161.001).
  • [ISSN] 1460-9568
  • [Journal-full-title] The European journal of neuroscience
  • [ISO-abbreviation] Eur. J. Neurosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Cholinergic Antagonists; 0 / Cholinesterase Inhibitors; 0 / Excitatory Amino Acid Antagonists; 0 / GABA Antagonists; 0 / Neurotransmitter Agents; 0 / Nicotinic Agonists; 3KX376GY7L / Glutamic Acid; 56-12-2 / gamma-Aminobutyric Acid; H9Y79VD43J / Strychnine; N9YNS0M02X / Acetylcholine
  •  go-up   go-down


62. Haeseleer F: Interaction and colocalization of CaBP4 and Unc119 (MRG4) in photoreceptors. Invest Ophthalmol Vis Sci; 2008 Jun;49(6):2366-75
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CaBP4 and Unc119 colocalized in the photoreceptor synapse of adult retina and during postnatal retinal development.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Invest Ophthalmol Vis Sci. 2001 Sep;42(10):2414-8 [11527958.001]
  • [Cites] Nat Genet. 1998 Jul;19(3):264-7 [9662400.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Jan 18;290(2):615-23 [11785943.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Feb;43(2):308-13 [11818371.001]
  • [Cites] Nat Neurosci. 2002 Mar;5(3):210-7 [11865310.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 May;43(5):1595-603 [11980879.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 28;99(11):7711-6 [12032348.001]
  • [Cites] Adv Exp Med Biol. 2002;514:303-17 [12596929.001]
  • [Cites] J Biol Chem. 2003 Mar 7;278(10):8837-45 [12496276.001]
  • [Cites] J Biol Chem. 2004 Jan 2;279(1):547-55 [14570872.001]
  • [Cites] EMBO J. 2004 Jan 28;23(2):312-21 [14685260.001]
  • [Cites] J Exp Med. 2004 Feb 2;199(3):369-79 [14757743.001]
  • [Cites] J Neurosci. 2004 May 12;24(19):4698-708 [15140941.001]
  • [Cites] J Bioenerg Biomembr. 1998 Aug;30(4):335-45 [9758330.001]
  • [Cites] Eur J Neurosci. 1999 Aug;11(8):2989-93 [10457194.001]
  • [Cites] J Biol Chem. 2004 Dec 10;279(50):52124-31 [15466855.001]
  • [Cites] J Biol Chem. 2004 Dec 17;279(51):53828-39 [15459196.001]
  • [Cites] Genesis. 2004 Dec;40(4):223-30 [15593328.001]
  • [Cites] J Biol Chem. 2005 Aug 12;280(32):29250-5 [15961391.001]
  • [Cites] Pflugers Arch. 2005 Aug;450(5):345-54 [15895247.001]
  • [Cites] Prog Retin Eye Res. 2005 Nov;24(6):682-720 [16027025.001]
  • [Cites] Hum Mol Genet. 2005 Oct 15;14(20):3035-46 [16155113.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Nov;46(11):4320-7 [16249514.001]
  • [Cites] Vis Neurosci. 2006 Jan-Feb;23(1):11-24 [16597347.001]
  • [Cites] Am J Hum Genet. 2006 Oct;79(4):657-67 [16960802.001]
  • [Cites] Cell Tissue Res. 2006 Nov;326(2):339-46 [16775698.001]
  • [Cites] J Biol Chem. 2000 Jan 14;275(2):1247-60 [10625670.001]
  • [Cites] J Neurogenet. 2000 Jan;13(4):191-212 [10858820.001]
  • [Cites] Microsc Res Tech. 2000 Jul 15;50(2):141-50 [10891878.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Oct;41(11):3268-77 [11006213.001]
  • [Cites] J Neurosci. 2006 Oct 18;26(42):10677-89 [17050707.001]
  • [Cites] Gene. 2007 Mar 1;389(1):45-51 [17123749.001]
  • [Cites] Exp Eye Res. 2007 Mar;84(3):473-85 [17174953.001]
  • [Cites] Nat Neurosci. 2004 Oct;7(10):1079-87 [15452577.001]
  • [Cites] J Comp Neurol. 1990 Nov 15;301(3):433-42 [2262600.001]
  • [Cites] Genetics. 1995 Nov;141(3):977-88 [8582641.001]
  • [Cites] J Biol Chem. 1996 Jan 19;271(3):1797-804 [8576185.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1998 Apr;39(5):690-8 [9538874.001]
  • [Cites] Nat Genet. 1998 Jul;19(3):260-3 [9662399.001]
  • [Cites] Development. 2001 Oct;128(20):4079-92 [11641230.001]
  • (PMID = 18296658.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY014561-03; United States / NEI NIH HHS / EY / R03 EY014561; United States / NEI NIH HHS / EY / EY014561; United States / NEI NIH HHS / EY / EY001730-31; United States / NEI NIH HHS / EY / P30 EY001730; United States / NEI NIH HHS / EY / EY01730; United States / NEI NIH HHS / EY / R03 EY014561-03; United States / NEI NIH HHS / EY / P30 EY001730-31
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Cabp4 protein, mouse; 0 / Calcium-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Microtubule Proteins; 0 / Nerve Tissue Proteins; 0 / Unc119 protein, mouse
  • [Other-IDs] NLM/ NIHMS105394; NLM/ PMC2670247
  •  go-up   go-down


63. Siu AW, Lau MK, Cheng JS, Chow CK, Tam WC, Li KK, Lee DK, To TS, To CH, Do CW: Glutamate-induced retinal lipid and protein damage: the protective effects of catechin. Neurosci Lett; 2008 Feb 27;432(3):193-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glutamate-induced retinal lipid and protein damage: the protective effects of catechin.
  • Glutamate toxicity has been implicated in various retinal diseases.
  • This study investigated the effects of catechin on the glutamate-treated retina.
  • Porcine retinal homogenates were incubated with glutamate (20 nmol) at 37 degrees C for 60 min.
  • Catechin was co-incubated with the glutamate-treated retina in the same condition.
  • Glutamate increased the retinal MDA (p<0.0001) and catechin reversed the effect (p<0.0001).
  • Our study shows that (a) retinal glutamate toxicity is mediated by LPO and protein modification, and (b) catechin ameliorates the toxicity.
  • [MeSH-major] Catechin / pharmacology. Glutamic Acid / toxicity. Lipid Peroxidation / drug effects. Retina / drug effects

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GLUTAMIC ACID HYDROCHLORIDE .
  • Hazardous Substances Data Bank. MALONALDEHYDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18249068.001).
  • [ISSN] 0304-3940
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Proteins; 3KX376GY7L / Glutamic Acid; 4Y8F71G49Q / Malondialdehyde; 8R1V1STN48 / Catechin
  •  go-up   go-down


64. Melbourne-Chambers R, Singh Minott I, Mowatt L, Johnson P, Thame M: Aicardi syndrome associated with anterior cephalocele in a female infant. Dev Med Child Neurol; 2007 Jun;49(6):464-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ophthalmological evaluation revealed left exotropia, dysplastic optic discs and retina, 'morning glory' appearance of the left optic disc, and bilateral chorioretinal lacunae.
  • [MeSH-major] Agenesis of Corpus Callosum. Choroid / abnormalities. Encephalocele / complications. Encephalocele / physiopathology. Ethmoid Sinus / abnormalities. Retina / abnormalities. Spasms, Infantile / complications

  • Genetic Alliance. consumer health - Aicardi Syndrome.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17518934.001).
  • [ISSN] 0012-1622
  • [Journal-full-title] Developmental medicine and child neurology
  • [ISO-abbreviation] Dev Med Child Neurol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


65. Abramowicz MJ, Ribai P, Cordonnier M: Congenital stationary night blindness: report of an autosomal recessive family and linkage analysis. Am J Med Genet A; 2005 Jan 1;132A(1):76-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Congenital stationary night blindness (CSNB) is a group of rare, non-progressive conditions of the retina characterized by abnormal rod function causing impaired night vision.
  • The latter determine lamina-specific connectivity in the retina, a histological substrate of the ON pathway implicated in complete, Schubert-Bornschein CSNB.

  • Genetic Alliance. consumer health - Night blindness, congenital stationary.
  • Genetic Alliance. consumer health - Blindness.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2004 Wiley-Liss, Inc.
  • (PMID = 15551339.001).
  • [ISSN] 1552-4825
  • [Journal-full-title] American journal of medical genetics. Part A
  • [ISO-abbreviation] Am. J. Med. Genet. A
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FMR1 protein, human; 0 / Nerve Tissue Proteins; 0 / RNA-Binding Proteins; 0 / Receptors, Androgen; 139135-51-6 / Fragile X Mental Retardation Protein
  •  go-up   go-down


66. Kalathur RK, Gagniere N, Berthommier G, Poidevin L, Raffelsberger W, Ripp R, Léveillard T, Poch O: RETINOBASE: a web database, data mining and analysis platform for gene expression data on retina. BMC Genomics; 2008;9:208
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RETINOBASE: a web database, data mining and analysis platform for gene expression data on retina.
  • BACKGROUND: The retina is a multi-layered sensory tissue that lines the back of the eye and acts at the interface of input light and visual perception.
  • Defects in any of these cells can lead to a variety of retinal diseases, including age-related macular degeneration, retinitis pigmentosa, Leber congenital amaurosis and glaucoma.
  • Recent progress in genomics and microarray technology provides extensive opportunities to examine alterations in retinal gene expression profiles during development and diseases.
  • However, there is no specific database that deals with retinal gene expression profiling.
  • In this context we have built RETINOBASE, a dedicated microarray database for retina.
  • DESCRIPTION: RETINOBASE is a microarray relational database, analysis and visualization system that allows simple yet powerful queries to retrieve information about gene expression in retina.
  • It provides access to gene expression meta-data and offers significant insights into gene networks in retina, resulting in better hypothesis framing for biological problems that can subsequently be tested in the laboratory.
  • Thus, RETINOBASE provides a framework to compare these methods and to optimize the retinal data analysis.
  • Overall, RETINOBASE provides efficient access to the global expression profiling of retinal genes from different organisms under various conditions.
  • [MeSH-major] Databases, Genetic. Gene Expression Profiling. Internet. Retina

  • FlyBase. FlyBase .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hum Mol Genet. 2006 Mar 1;15(5):691-703 [16434483.001]
  • [Cites] Glia. 2005 Dec;52(4):309-24 [16078232.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 7;103(10):3890-5 [16505381.001]
  • [Cites] Hum Mol Genet. 2006 Sep 1;15(17):2588-602 [16868010.001]
  • [Cites] Methods Enzymol. 2006;411:134-93 [16939790.001]
  • [Cites] FASEB J. 2006 Oct;20(12):2036-49 [17012256.001]
  • [Cites] Genes Dev. 2000 Apr 15;14(8):963-80 [10783168.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 May 9;97(10):5551-6 [10805811.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 2;98(1):31-6 [11134512.001]
  • [Cites] Bioinformatics. 2001 Apr;17(4):309-18 [11301299.001]
  • [Cites] Nat Neurosci. 2001 Sep;4(9):877-86 [11528418.001]
  • [Cites] Nat Genet. 2001 Dec;29(4):365-71 [11726920.001]
  • [Cites] Cell. 2001 Nov 30;107(5):579-89 [11733058.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Apr 2;99(7):4465-70 [11904358.001]
  • [Cites] Genome Biol. 2002 Jul 15;3(8):SOFTWARE0003 [12186655.001]
  • [Cites] Bioinformatics. 2002 Sep;18(9):1194-206 [12217911.001]
  • [Cites] Nucleic Acids Res. 2002 Sep 15;30(18):3992-4000 [12235383.001]
  • [Cites] Bioinformatics. 2002 Dec;18(12):1585-92 [12490442.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):4024-9 [12655063.001]
  • [Cites] Biostatistics. 2003 Apr;4(2):249-64 [12925520.001]
  • [Cites] Bioinformatics. 2003 Sep 22;19(14):1787-99 [14512350.001]
  • [Cites] Nat Genet. 2004 Apr;36(4):351-60 [14991054.001]
  • [Cites] Gene. 2004 Jun 23;335:159-68 [15194199.001]
  • [Cites] Hum Mol Genet. 2004 Jul 15;13(14):1487-503 [15163632.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Aug;45(8):2737-46 [15277499.001]
  • [Cites] PLoS Biol. 2004 Sep;2(9):E247 [15226823.001]
  • [Cites] Genome Biol. 2004;5(10):R80 [15461798.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Oct 1;88(19):8322-6 [1656438.001]
  • [Cites] Science. 1995 Oct 20;270(5235):484-7 [7570003.001]
  • [Cites] Nucleic Acids Res. 2007 Jan;35(Database issue):D760-5 [17099226.001]
  • [Cites] Nucleic Acids Res. 2007 Jan;35(Database issue):D747-50 [17132828.001]
  • [Cites] BMC Bioinformatics. 2006;7 Suppl 4:S17 [17217509.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2007 Feb;48(2):881-90 [17251491.001]
  • [Cites] Hum Mutat. 2007 Jul;28(7):741-2 [17584859.001]
  • [Cites] Bioinformatics. 2008 Jan 15;24(2):276-8 [18037684.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D533-6 [15608255.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D573-9 [15608264.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Jan;46(1):349-57 [15623795.001]
  • [Cites] J Neurosci. 2005 Jan 5;25(1):118-29 [15634773.001]
  • [Cites] Mol Vis. 2005 Feb 28;11:152-62 [15765048.001]
  • [Cites] Bioinformatics. 2005 May 15;21(10):2552-3 [15746287.001]
  • [Cites] Genome Biol. 2005;6(6):R48 [15960800.001]
  • [Cites] Bioinformatics. 2005 Sep 15;21(18):3683-5 [16076888.001]
  • [Cites] Hum Mol Genet. 2005 Oct 1;14(19):2945-58 [16126734.001]
  • [Cites] Genome Biol. 2005;6(9):R74 [16168081.001]
  • [Cites] Mol Vis. 2005;11:775-91 [16205622.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Mar;47(3):977-85 [16505032.001]
  • (PMID = 18457592.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2386825
  •  go-up   go-down


67. Venkataraman ST, Flanagan JG, Hudson C: Vascular reactivity of optic nerve head and retinal blood vessels in glaucoma--a review. Microcirculation; 2010 Oct;17(7):568-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vascular reactivity of optic nerve head and retinal blood vessels in glaucoma--a review.
  • Glaucoma is characterized by loss of retinal nerve fibers, structural changes to the optic nerve, and an associated change in visual function.
  • It has been proposed that primary open angle glaucoma could be associated with structural abnormalities and/or functional dysregulation of the vasculature supplying the optic nerve and surrounding retinal tissue.
  • Under normal conditions, blood flow is autoregulated, i.e., maintained at a relatively constant level, in the retina and ONH, irrespective of variation in ocular perfusion pressure.
  • A number of factors released by the vascular endothelium, including endothelin-1 and nitric oxide, are suggested to play an important role in the regulation of local perfusion in the retina and ONH.
  • [MeSH-major] Glaucoma / physiopathology. Optic Disk / blood supply. Retinal Vessels / physiopathology

  • Genetic Alliance. consumer health - Glaucoma.
  • MedlinePlus Health Information. consumer health - Glaucoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 John Wiley & Sons Ltd.
  • (PMID = 21040122.001).
  • [ISSN] 1549-8719
  • [Journal-full-title] Microcirculation (New York, N.Y. : 1994)
  • [ISO-abbreviation] Microcirculation
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  •  go-up   go-down


68. Witkovsky P, Gábriel R, Krizaj D: Anatomical and neurochemical characterization of dopaminergic interplexiform processes in mouse and rat retinas. J Comp Neurol; 2008 Sep 10;510(2):158-74
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Dopaminergic (DA) neurons of mouse and rat retinas are of the interplexiform subtype (DA-IPC), i.e., they send processes distally toward the outer retina, exhibiting numerous varicosities along their course.
  • The primary question we addressed was whether distally located DA-IPC varicosities, identified by tyrosine hydroxylase (TH) immunoreactivity, had the characteristic presynaptic proteins associated with calcium-dependent vesicular release of neurotransmitter.
  • We found that TH immunoreactive varicosities in the outer retina possessed vesicular monoamine transporter 2 and vesicular GABA transporter, but they lacked immunostaining for any of nine subtypes of voltage-dependent calcium channel.
  • Immunoreactivity for other channels that may permit calcium influx such as certain ionotropic glutamate receptors and canonical transient receptor potential channels (TRPCs) was similarly absent, although DA-IPC varicosities did show ryanodine receptor immunoreactivity, indicating the presence of intracellular calcium stores.
  • The synaptic vesicle proteins sv2a and sv2b and certain other proteins associated with the presynaptic membrane were absent from DA-IPC varicosities, but the vesicular SNARE protein, vamp2, was present in a fraction of those varicosities.
  • Outer retinal varicosities of this putative GABAergic IPC did colocalize synaptic vesicle protein 2a, suggesting they possessed a conventional vesicular release mechanism.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOPAMINE .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • SciCrunch. The Antibody Registry: Reagent: Antibodies .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • [Cites] J Gen Physiol. 2002 Apr;119(4):373-88 [11929887.001]
  • [Cites] Cell Calcium. 2007 Aug;42(2):157-62 [17517435.001]
  • [Cites] J Neurophysiol. 2002 Nov;88(5):2765-77 [12424311.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1358-63 [12547914.001]
  • [Cites] J Comp Neurol. 2003 May 19;460(1):106-22 [12687700.001]
  • [Cites] Neuroscience. 2003;118(3):763-8 [12710983.001]
  • [Cites] J Vis. 2003;3(4):274-80 [12803536.001]
  • [Cites] Annu Rev Neurosci. 2003;26:701-28 [14527272.001]
  • [Cites] Pharmacol Rev. 2003 Dec;55(4):579-81 [14657414.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):16065-70 [14668438.001]
  • [Cites] J Neurosci. 2004 Feb 18;24(7):1707-18 [14973233.001]
  • [Cites] Doc Ophthalmol. 2004 Jan;108(1):17-40 [15104164.001]
  • [Cites] Trends Neurosci. 2004 May;27(5):270-7 [15111009.001]
  • [Cites] J Neurosci. 2004 Apr 28;24(17):4242-9 [15115820.001]
  • [Cites] J Comp Neurol. 2004 Aug 2;475(4):463-80 [15236230.001]
  • [Cites] Science. 1975 Apr 18;188(4185):270-3 [804181.001]
  • [Cites] Proc R Soc Lond B Biol Sci. 1975 Dec 2;191(1104):353-68 [2921.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Jan;77(1):658-61 [6928650.001]
  • [Cites] Brain Res. 1980 Sep 8;196(2):365-72 [6249448.001]
  • [Cites] J Comp Neurol. 1982 Sep 1;210(1):65-79 [6127354.001]
  • [Cites] Brain Res Bull. 1982 Jul-Dec;9(1-6):379-81 [6129041.001]
  • [Cites] J Histochem Cytochem. 1983 Feb;31(2):285-92 [6339606.001]
  • [Cites] Vision Res. 1971;Suppl 3:33-50 [4951186.001]
  • [Cites] J Neurosci. 1988 Sep;8(9):3383-94 [2902202.001]
  • [Cites] J Comp Neurol. 1988 Aug 22;274(4):608-18 [2906071.001]
  • [Cites] J Neurocytol. 1990 Jun;19(3):343-66 [2391538.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Mar 15;90(6):2150-4 [7681585.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Jun 15;90(12):5667-71 [8516316.001]
  • [Cites] J Comp Neurol. 1995 Mar 20;353(4):553-71 [7759615.001]
  • [Cites] Brain Res. 1995 Apr 10;676(2):363-70 [7614007.001]
  • [Cites] J Comp Neurol. 2000 Aug 14;424(1):1-23 [10888735.001]
  • [Cites] Nat Neurosci. 2000 Dec;3(12):1256-65 [11100146.001]
  • [Cites] Neuron. 2000 Dec;28(3):847-56 [11163271.001]
  • [Cites] Neuron. 2001 Apr;30(1):211-25 [11343656.001]
  • [Cites] J Neurosci. 2001 Jul 1;21(13):4543-50 [11425883.001]
  • [Cites] J Neurosci. 1995 Sep;15(9):6179-88 [7666200.001]
  • [Cites] J Neurosci. 1996 Jul 1;16(13):4135-45 [8753875.001]
  • [Cites] J Neurosci. 1996 Nov 1;16(21):6713-21 [8824312.001]
  • [Cites] J Comp Neurol. 1996 Nov 11;375(2):212-24 [8915826.001]
  • [Cites] J Chem Neuroanat. 1996 Nov;12(1):37-50 [9001947.001]
  • [Cites] J Neurophysiol. 1997 Feb;77(2):853-62 [9065854.001]
  • [Cites] Neuron. 1997 May;18(5):723-36 [9182798.001]
  • [Cites] Mol Neurobiol. 1999 Jun;19(3):181-204 [10495103.001]
  • [Cites] J Comp Neurol. 2005 Jan 24;481(4):352-62 [15593337.001]
  • [Cites] J Neurophysiol. 2005 Dec;94(6):4196-208 [16293593.001]
  • [Cites] J Neurochem. 2006 Feb;96(3):645-55 [16405515.001]
  • [Cites] Trends Pharmacol Sci. 2006 Feb;27(2):78-84 [16412523.001]
  • [Cites] J Neurosci. 2006 Feb 8;26(6):1759-66 [16467524.001]
  • [Cites] Neuroreport. 2006 May 29;17(8):773-7 [16708013.001]
  • [Cites] J Comp Neurol. 2006 Jul 20;497(3):384-96 [16736476.001]
  • [Cites] Nature. 2006 Oct 12;443(7112):705-8 [17036006.001]
  • [Cites] Cell Calcium. 2006 Nov-Dec;40(5-6):495-504 [17030060.001]
  • [Cites] J Comp Neurol. 2002 May 27;447(2):138-51 [11977117.001]
  • (PMID = 18615559.001).
  • [ISSN] 1096-9861
  • [Journal-full-title] The Journal of comparative neurology
  • [ISO-abbreviation] J. Comp. Neurol.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY013870-07; United States / NEI NIH HHS / EY / R01 EY013870; United States / NEI NIH HHS / EY / EY 13870; United States / NEI NIH HHS / EY / R01 EY013870-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ryanodine Receptor Calcium Release Channel; 0 / Sodium Channels; EC 1.14.16.2 / Tyrosine 3-Monooxygenase; SY7Q814VUP / Calcium; VTD58H1Z2X / Dopamine
  • [Other-IDs] NLM/ NIHMS227029; NLM/ PMC2923661
  •  go-up   go-down


69. Shields CL, Perez B, Benavides R, Materin MA, Shields JA: Optical coherence tomography of optic disk melanocytoma in 15 cases. Retina; 2008 Mar;28(3):441-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MAIN OUTCOME MEASURES: OCT characteristics of the tumor.
  • By ophthalmoscopy, the mean basal diameter of the tumor was 2.7 mm, and by ultrasonography, the mean thickness was 1.8 mm.
  • By OCT, the tumor showed a nodular appearance in 14 cases (93%).
  • The tumor displayed a gradual sloping transition from normal retina into the mass, hyperreflectivity at its anterior tumor surface, and dense posterior shadowing with an optically empty appearance in all 15 cases (100%).
  • There were no internal qualities of the tumor or disk visible by OCT due to dense shadowing.
  • Other findings of OCT included vitreous seeds in 2 cases (13%) and adjacent retinal edema in 1 case (7%).
  • There were no cases of retinal traction, subretinal fluid, macular edema, or epiretinal membrane in the macula.
  • CONCLUSIONS: Optic disk melanocytoma shows characteristic features by OCT including a gradual transition from normal retina into nodular tumor, and the mass displays a bright anterior border layer with optically empty internal details.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18327136.001).
  • [ISSN] 0275-004X
  • [Journal-full-title] Retina (Philadelphia, Pa.)
  • [ISO-abbreviation] Retina (Philadelphia, Pa.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


70. Bennicelli J, Wright JF, Komaromy A, Jacobs JB, Hauck B, Zelenaia O, Mingozzi F, Hui D, Chung D, Rex TS, Wei Z, Qu G, Zhou S, Zeiss C, Arruda VR, Acland GM, Dell'Osso LF, High KA, Maguire AM, Bennett J: Reversal of blindness in animal models of leber congenital amaurosis using optimized AAV2-mediated gene transfer. Mol Ther; 2008 Mar;16(3):458-65
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Immunohistochemistry confirmed transduction of retinal pigment epithelium cells and there was minimal toxicity to the retina as judged by histopathologic analysis.

  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • SciCrunch. OMIA - Online Mendelian Inheritance in Animals: Data: Gene Expression .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hum Mol Genet. 2002 May 15;11(10):1169-76 [12015276.001]
  • [Cites] Nat Genet. 2001 May;28(1):92-5 [11326284.001]
  • [Cites] J Hered. 2003 Jan-Feb;94(1):31-7 [12692160.001]
  • [Cites] Prog Retin Eye Res. 2003 Sep;22(5):683-703 [12892646.001]
  • [Cites] Doc Ophthalmol. 2003 Jul;107(1):79-86 [12906125.001]
  • [Cites] Mol Ther. 2004 Feb;9(2):182-8 [14759802.001]
  • [Cites] Hum Mutat. 2004 Apr;23(4):306-17 [15024725.001]
  • [Cites] Br J Ophthalmol. 1989 Sep;73(9):750-6 [2804031.001]
  • [Cites] J Neurosci. 1996 Jan 15;16(2):563-71 [8551340.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1997 Dec;38(13):2857-63 [9418740.001]
  • [Cites] Mol Vis. 1998 Oct 30;4:23 [9808841.001]
  • [Cites] J Neurosci. 1999 Jan 1;19(1):442-55 [9870972.001]
  • [Cites] Genomics. 1999 Apr 1;57(1):57-61 [10191083.001]
  • [Cites] Mol Vis. 2005 Feb 28;11:152-62 [15765048.001]
  • [Cites] Mol Ther. 2005 Dec;12(6):1072-82 [16226919.001]
  • [Cites] Vis Neurosci. 2005 Sep-Oct;22(5):677-84 [16332278.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Jul;47(7):2865-75 [16799026.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Dec 19;103(51):19541-5 [17159157.001]
  • [Cites] Nat Genet. 2007 Jul;39(7):889-95 [17546029.001]
  • [Cites] Methods Enzymol. 2000;316:705-24 [10800710.001]
  • [Cites] Methods Enzymol. 2000;316:777-89 [10800714.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Apr;44(4):1663-72 [12657607.001]
  • (PMID = 18209734.001).
  • [ISSN] 1525-0024
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / R01 EY010820-13; United States / NEI NIH HHS / EY / R01 EY006855; United States / NEI NIH HHS / EY / EY06855; United States / NEI NIH HHS / EY / EY10820; United States / NEI NIH HHS / EY / EY015398; United States / NEI NIH HHS / EY / K12 EY015398; United States / NEI NIH HHS / EY / R01 EY010820; United States / NEI NIH HHS / EY / R01 EY010820-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Eye Proteins; EC 3.1.1.64 / retinoid isomerohydrolase; EC 5.2.- / cis-trans-Isomerases
  • [Other-IDs] NLM/ NIHMS176415; NLM/ PMC2842085
  •  go-up   go-down


71. Stieger K, Mendes-Madeira A, Meur GL, Weber M, Deschamps JY, Nivard D, Provost N, Moullier P, Rolling F: Oral administration of doxycycline allows tight control of transgene expression: a key step towards gene therapy of retinal diseases. Gene Ther; 2007 Dec;14(23):1668-73
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oral administration of doxycycline allows tight control of transgene expression: a key step towards gene therapy of retinal diseases.
  • Gene transfer of neurotrophic or antiangiogenic factors has been shown to improve photoreceptor survival in retinal degenerative disorders (that is retinitis pigmentosa) and to prevent neovascularization in retinal vascular diseases (that is age-related macular degeneration, diabetic retinopathy).
  • In a previous study, we demonstrated that rAAV-mediated gene transfer of the tetracycline-regulatable (tetR) system allows transgene regulation in the retina of nonhuman primates after intravenous administration of doxycycline (Dox).
  • The purpose of this study was to evaluate oral administration of Dox to control transgene expression in the retina, since the pharmacokinetics after oral administration of the inducer drug represent a key factor when considering advancing to clinical trials.
  • [MeSH-major] Anti-Bacterial Agents / administration & dosage. Doxycycline / administration & dosage. Genetic Therapy / methods. Retinal Diseases / therapy
  • [MeSH-minor] Administration, Oral. Animals. Dependovirus / genetics. Dose-Response Relationship, Drug. Erythropoietin / analysis. Erythropoietin / genetics. Gene Expression / drug effects. Genetic Vectors / administration & dosage. Genetic Vectors / genetics. Macaca. Models, Animal. Retina / chemistry. Transgenes

  • MedlinePlus Health Information. consumer health - Antibiotics.
  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • Hazardous Substances Data Bank. DOXYCYCLINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17914405.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 11096-26-7 / Erythropoietin; N12000U13O / Doxycycline
  •  go-up   go-down


72. Denny CA, Alroy J, Pawlyk BS, Sandberg MA, d'Azzo A, Seyfried TN: Neurochemical, morphological, and neurophysiological abnormalities in retinas of Sandhoff and GM1 gangliosidosis mice. J Neurochem; 2007 Jun;101(5):1294-302
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Retinal abnormalities are well documented in patients with ganglioside storage diseases.
  • The total content and distribution of retinal glycosphingolipids was studied for the first time in control mice and in Sandhoff disease (SD) and GM1 gangliosidosis mice.
  • Similar to previous findings in rat retina, GD3 was the major ganglioside in mouse retina, while GM2 and GM1 were minor species.
  • Our findings present a model system for assessing retinal pathobiology and therapies for the gangliosidoses.
  • [MeSH-major] Gangliosidosis, GM1 / genetics. Retina / metabolism. Retina / pathology. Sandhoff Disease / pathology. Sandhoff Disease / physiopathology

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17442056.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY016350; United States / NICHD NIH HHS / HD / HD39722; United States / NIDDK NIH HHS / DK / R01-DK52025
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.2.1.23 / beta-Galactosidase; EC 3.2.1.52 / beta-N-Acetylhexosaminidases
  •  go-up   go-down


73. Zamiri P, Sugita S, Streilein JW: Immunosuppressive properties of the pigmented epithelial cells and the subretinal space. Chem Immunol Allergy; 2007;92:86-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The PE cells of the iris, ciliary body, and retina reside in anatomically disparate locations and serve distinctly different functions, yet share interesting immunomodulatory properties that contribute to ocular immune privilege.
  • PE cells in the ciliary body and retina elaborate a variety of soluble factors that either directly or indirectly dampen immune-mediated inflammation; these include transforming growth factor-Beta, somatostatin, thrombospondin and pigment epithelial derived factor (PEDF).
  • The prospect of therapeutic retinal transplantation and the possible immunologic etiology for some forms of age-related macular degeneration provides new impetus for gaining a better understanding of ocular immune privilege in the posterior regions of the eye.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17264485.001).
  • [ISSN] 1660-2242
  • [Journal-full-title] Chemical immunology and allergy
  • [ISO-abbreviation] Chem Immunol Allergy
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Thrombospondin 1; 0 / Transforming Growth Factor beta
  • [Number-of-references] 48
  •  go-up   go-down


74. Santiago AR, Pereira TS, Garrido MJ, Cristóvão AJ, Santos PF, Ambrósio AF: High glucose and diabetes increase the release of [3H]-D-aspartate in retinal cell cultures and in rat retinas. Neurochem Int; 2006 May-Jun;48(6-7):453-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High glucose and diabetes increase the release of [3H]-D-aspartate in retinal cell cultures and in rat retinas.
  • Several evidences suggest that glutamate may be involved in retinal neurodegeneration in diabetic retinopathy (DR).
  • The accumulation of [(3)H]-D-aspartate did not change in cultured retinal neural cells treated with high glucose (30 mM) for 7 days.
  • However, the release of [(3)H]-D-aspartate, evoked by 50 mM KCl, significantly increased in retinal cells exposed to high glucose.
  • These results suggest that high glucose and diabetes increase the evoked release of D-aspartate in the retina, which may be correlated with the hypothesis of glutamate-induced retinal neurodegeneration in DR.
  • [MeSH-major] Aspartic Acid / metabolism. Diabetes Mellitus, Experimental / metabolism. Glucose / metabolism. Retina / metabolism