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[Title] Effect of PEL exopolysaccharide on the wspF mutant phenotypes in Pseudomonas aeruginosa PA14.

Here, we characterized the role of cyclic diguanylate (c-di-GMP) and EPS (PEL) overproduction in the wspF mutant phenotypes of P. aeruginosa PA14 (wrinkly appearance, hyperadherence, impaired motilities, and reduced virulence in acute infections).

We confirmed that the elevated c-di-GMP level plays a key role in all the wspF mutant phenotypes listed above, as assessed by ectopic expression of a c-di-GMP-degrading phophodiesterase (PvrR) in the wspF mutant.

In contrast, PEL EPS, which is overproduced in the wspF mutant, was necessary for wrinkly appearance and hyperadherence, but not for the impaired flagellar motilities and the attenuated virulence of the wspF mutant.

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(PMID = 18667850.001).

[ISSN] 1017-7825

[Journal-full-title] Journal of microbiology and biotechnology

[ISO-abbreviation] J. Microbiol. Biotechnol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Korea (South)

[Chemical-registry-number] 0 / Bacterial Proteins; 0 / Polysaccharides, Bacterial; 61093-23-0 / bis(3',5')-cyclic diguanylic acid; EC 3.1.- / Esterases; H2D2X058MU / Cyclic GMP

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cysteine residues in the large extracellular loop (EC2) are essential for the function of the stress-regulated glycoprotein M6a.

Gpm6a was identified as a stress-responsive gene in the hippocampal formation.

This gene is down-regulated in the hippocampus of both socially and physically stressed animals, and this effect can be reversed by antidepressant treatment.

Previously we showed that the stress-regulated protein M6a is a key modulator for neurite outgrowth and filopodium/spine formation.

In the present work, mutational analysis was used to characterize the action of M6a at the molecular level.

The presence of cysteines 162 and 202 is essential for the efficient cell surface expression of the M6a protein.

In contrast, cysteines 174 and 192, which form a disulfide bridge as shown by biochemical analysis, are not required for the efficient surface expression of M6a.

Their mutation to alanine does not interfere with the localization of M6a to filopodial protrusions in primary hippocampal neurons.

In non-permeabilized cells, these mutant proteins are not recognized by a function-blocking monoclonal antibody directed to M6a.

Taken together, this study demonstrates that cysteines in the EC2 domain are critical for the role of M6a in filopodium outgrowth and synaptogenesis.

Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

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[Cites] Biochem J. 2000 Nov 1;351 Pt 3:629-37 [11042117.001]

[Cites] Neuroscience. 2000;97(2):253-66 [10799757.001]

[Cites] EMBO J. 2001 Jan 15;20(1-2):12-8 [11226150.001]

[Cites] J Biol Chem. 2001 Feb 16;276(7):4853-62 [11087758.001]

[Cites] J Biol Chem. 2001 Jul 6;276(27):25005-13 [11325968.001]

[Cites] Virus Res. 2001 Nov 28;80(1-2):1-10 [11597743.001]

[Cites] J Biol Chem. 2001 Oct 26;276(43):40055-64 [11483611.001]

[Cites] J Biol Chem. 2001 Nov 2;276(44):40545-54 [11504738.001]

[Cites] J Cell Sci. 2001 Dec;114(Pt 23):4143-51 [11739647.001]

[Cites] Mol Cell Neurosci. 2001 Dec;18(6):593-605 [11749036.001]

[Cites] J Neurosci. 2002 Sep 1;22(17):7398-407 [12196561.001]

[Cites] J Cell Biol. 2002 Sep 30;158(7):1299-309 [12356873.001]

[Cites] Biochem Biophys Res Commun. 2002 Oct 4;297(4):722-8 [12359212.001]

[Cites] Science. 2002 Oct 25;298(5594):770-6 [12399577.001]

[Cites] Trends Biochem Sci. 2003 Feb;28(2):106-12 [12575999.001]

[Cites] Eur J Neurosci. 2003 Jun;17(11):2447-56 [12814376.001]

[Cites] Trends Immunol. 2003 Nov;24(11):610-7 [14596886.001]

[Cites] J Neurosci Res. 2003 Dec 1;74(5):744-53 [14635225.001]

[Cites] Biochem J. 2004 Jan 15;377(Pt 2):407-17 [14556650.001]

[Cites] Eur J Neurosci. 2004 Feb;19(3):659-66 [14984416.001]

[Cites] J Neurosci. 1991 Jun;11(6):1617-26 [1904480.001]

[Cites] J Neurobiol. 1992 Feb;23(1):71-88 [1564456.001]

[Cites] Biochemistry. 1992 Dec 15;31(49):12289-96 [1281423.001]

[Cites] Neuron. 1993 Sep;11(3):423-31 [8398137.001]

[Cites] Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):4029-33 [8171030.001]

[Cites] EMBO J. 1994 May 15;13(10):2322-30 [8194524.001]

[Cites] Neuroscience. 1995 Nov;69(1):83-8 [8637635.001]

[Cites] Neuroscience. 1995 Nov;69(1):89-98 [8637636.001]

[Cites] J Comp Neurol. 1996 Jul 8;370(4):465-78 [8807448.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):14002-8 [9391142.001]

[Cites] Acta Anat (Basel). 1998;162(2-3):75-84 [9831753.001]

[Cites] Biochem J. 1999 May 15;340 ( Pt 1):103-11 [10229664.001]

[Cites] J Neurocytol. 1998 Sep;27(9):695-703 [10447243.001]

[Cites] Nat Rev Immunol. 2005 Feb;5(2):136-48 [15688041.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Feb 8;102(6):1939-44 [15677332.001]

[Cites] Physiology (Bethesda). 2005 Aug;20:218-24 [16024509.001]

[Cites] BMC Struct Biol. 2005;5:11 [15985154.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Nov 22;102(47):17196-201 [16286650.001]

[Cites] Nat Rev Mol Cell Biol. 2005 Oct;6(10):801-11 [16314869.001]

[Cites] Biol Psychiatry. 2006 Feb 1;59(3):244-51 [16140276.001]

[Cites] Neuroscience. 2006 Jun 30;140(2):597-606 [16600515.001]

[Cites] Mol Cell Biol. 2006 Oct;26(20):7707-18 [16908530.001]

[Cites] J Biol Chem. 2007 Jul 27;282(30):22239-47 [17548356.001]

[Cites] Mol Cell Proteomics. 2007 Nov;6(11):1855-67 [17644758.001]

[Cites] Brain Res. 2008 Mar 4;1197:1-12 [18241840.001]

[Cites] Am J Med Genet B Neuropsychiatr Genet. 2008 Sep 5;147B(6):707-11 [18163405.001]

[Cites] Mol Vis. 2008;14:1623-30 [18776950.001]

[Cites] Stem Cells Dev. 2008 Aug;17(4):641-51 [18522499.001]

[Cites] Nat Genet. 2000 Feb;24(2):167-70 [10655063.001]

[Cites] J Virol. 2000 Apr;74(8):3642-9 [10729140.001]

[Cites] Int J Dev Biol. 2000;44(6):725-31 [11061437.001]

(PMID = 19737934.001).

[ISSN] 1083-351X

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Gpm6a protein, rat; 0 / Membrane Glycoproteins; 0 / Nerve Tissue Proteins; K848JZ4886 / Cysteine

[Other-IDs] NLM/ PMC2797278

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] M6a is expressed in the murine neural retina and regulates neurite extension.

PURPOSE: Glycoprotein m6a (M6a) is a cell-surface glycoprotein that belongs to the myelin proteolipid protein family.

M6a is expressed mainly in the nervous system, and its expression and function in mammalian retina have not been described.

Using proteomics analysis of mouse retinal membrane fractions, we identified M6a as a retinal membrane protein that is strongly expressed at embryonic stages.

Our aim was to reveal the function of M6a in development of mouse retina in this work.

METHODS: Detailed expression pattern of M6a was examined by immunostaining using frozen sections of mouse retina obtained at various developmental stages.

For functional analysis of M6a in mouse retinal development, we performed retorovirus-mediated overexpression of M6a in mouse retinal explant culture.

RESULTS: M6a transcripts were strongly expressed in embryonic retina.

After completion of retinal differentiation, the level of expression decreased as mouse development progressed.

Immunohistochemistry showed that in the immature mouse retina, M6a was strongly expressed in the axons of retinal ganglion cells.

After birth, M6a expression was confined to the inner plexiform layer, and finally, to the inner and outer plexiform layers of adult mouse retina.

M6a expression was completely paralleled by that of the synaptic marker, synaptophysin.

Mouse retinal progenitor cells that overexpressed M6a following retrovirus-mediated gene transfer were subjected to in vitro explant or monolayer cultures.

The neurite outgrowth of M6a-overexpressing retinal cells was strikingly enhanced, although M6a did not affect differentiation and proliferation.

CONCLUSIONS: These results suggest that M6a plays a role in retinal development by regulating neurites, and it may also function to modulate synaptic activities in the adult retina.

[MeSH-minor] Animals. Biomarkers / metabolism. Cell Differentiation. Cell Lineage. Cell Proliferation. Gene Expression Regulation, Developmental. Mice. Mice, Inbred ICR. Mitosis. Protein Transport. Stem Cells / cytology. Stem Cells / metabolism. Synapses / metabolism

Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

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[Cites] Dev Biol. 2007 Jan 1;301(1):141-54 [17069792.001]

[Cites] Dev Biol. 2006 Apr 1;292(1):265-76 [16499901.001]

[Cites] Nature. 2000 Jan 6;403(6765):93-8 [10638760.001]

[Cites] Gene Ther. 2000 Jun;7(12):1063-6 [10871756.001]

[Cites] Trends Neurosci. 2002 Jan;25(1):32-8 [11801336.001]

[Cites] J Neurosci. 2002 Sep 1;22(17):7398-407 [12196561.001]

[Cites] Biochem Biophys Res Commun. 2002 Oct 4;297(4):722-8 [12359212.001]

[Cites] Brain Res Dev Brain Res. 2003 Oct 10;145(1):93-105 [14519497.001]

[Cites] Mol Cell Biol. 2004 May;24(10):4513-21 [15121868.001]

[Cites] Int J Cancer. 1983 Jan 15;31(1):13-20 [6339421.001]

[Cites] J Neurosci. 1991 Jun;11(6):1617-26 [1904480.001]

[Cites] J Neurobiol. 1992 Feb;23(1):71-88 [1564456.001]

[Cites] Dev Dyn. 1992 Aug;194(4):311-25 [1286213.001]

[Cites] Neuron. 1993 Sep;11(3):423-31 [8398137.001]

[Cites] Neuron. 1994 Mar;12(3):583-95 [7512350.001]

[Cites] J Comp Neurol. 1996 Jul 8;370(4):465-78 [8807448.001]

[Cites] Mech Dev. 1998 Aug;76(1-2):3-18 [9767078.001]

[Cites] J Neurosci Res. 1999 Jul 1;57(1):13-22 [10397631.001]

[Cites] J Neurocytol. 1998 Sep;27(9):695-703 [10447243.001]

[Cites] J Cell Sci. 2005 Oct 1;118(Pt 19):4473-83 [16179606.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Nov 22;102(47):17196-201 [16286650.001]

[Cites] Biochem J. 2007 Nov 15;408(1):51-9 [17688421.001]

(PMID = 18776950.001).

[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] 0 / Biomarkers; 0 / Gpm6a protein, mouse; 0 / Membrane Glycoproteins; 0 / Nerve Tissue Proteins

[Other-IDs] NLM/ PMC2529470

   

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Expression of the axonal membrane glycoprotein M6a is regulated by chronic stress.

The present study shows that chronic stress also regulates expression of M6a, a glycoprotein which is localised in axonal membranes.

We have previously demonstrated that M6a is a component of glutamatergic axons.

The present data reveal that it is the splice variant M6a-Ib, not M6a-Ia, which is strongly expressed in the brain.

Chronic stress in male rats (3 weeks daily restraint) has regional effects: quantitative in situ hybridization demonstrated that M6a-Ib mRNA in dentate gyrus granule neurons and in CA3 pyramidal neurons is downregulated, whereas M6a-Ib mRNA in the medial prefrontal cortex is upregulated by chronic stress.

Enhanced M6a-Ib expression in the medial prefrontal cortex (in areas prelimbic and infralimbic cortex) might be interpreted as a compensatory mechanism in response to changes in axonal projections from the hippocampus.

[MeSH-major] Axons / metabolism. Brain / metabolism. Gene Expression Regulation. Membrane Glycoproteins / genetics. Nerve Tissue Proteins / genetics. Stress, Physiological / physiology

[MeSH-minor] Animals. Down-Regulation. Gene Expression. In Situ Hybridization. Kidney / metabolism. Male. Neurons / metabolism. Protein Isoforms. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Restraint, Physical

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[Cites] Neuroscience. 2000;97(2):253-66 [10799757.001]

[Cites] Behav Brain Res. 2008 Jun 26;190(1):1-13 [18384891.001]

[Cites] Mol Cell Neurosci. 2001 Dec;18(6):593-605 [11749036.001]

[Cites] Hippocampus. 2002;12(2):245-57 [12000121.001]

[Cites] Neurosci Biobehav Rev. 2002 May;26(3):321-52 [12034134.001]

[Cites] J Neuroendocrinol. 2002 Jun;14(6):499-505 [12047725.001]

[Cites] Eur J Neurosci. 2004 Feb;19(3):659-66 [14984416.001]

[Cites] Neuroscience. 2004;125(1):1-6 [15051139.001]

[Cites] BMC Genomics. 2003 Jul 29;4(1):31 [12885301.001]

[Cites] J Neurobiol. 2004 Aug;60(2):236-48 [15266654.001]

[Cites] Stress. 2004 Jun;7(2):131-43 [15512858.001]

[Cites] J Comp Neurol. 1977 Mar 1;172(1):49-84 [65364.001]

[Cites] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5665-9 [2441390.001]

[Cites] Brain Res Bull. 1987 Dec;19(6):639-49 [2449937.001]

[Cites] Neuroscience. 1988 Feb;24(2):379-431 [2452377.001]

[Cites] J Neurobiol. 1992 Feb;23(1):71-88 [1564456.001]

[Cites] Brain Res. 1992 Aug 21;588(2):341-5 [1393587.001]

[Cites] J Neurosci. 1993 Sep;13(9):3839-47 [8396170.001]

[Cites] Neuron. 1993 Sep;11(3):423-31 [8398137.001]

[Cites] J Neurochem. 1993 Nov;61(5):1957-60 [7901339.001]

[Cites] Hippocampus. 1993;3 Spec No:33-44 [8287110.001]

[Cites] Neuroscience. 1995 Nov;69(1):83-8 [8637635.001]

[Cites] J Neurosci. 1996 May 15;16(10):3534-40 [8627386.001]

[Cites] J Comp Neurol. 1996 Jul 8;370(4):465-78 [8807448.001]

[Cites] J Comp Neurol. 1997 Jan 27;377(4):465-99 [9007187.001]

[Cites] Anal Biochem. 1997 Feb 15;245(2):154-60 [9056205.001]

[Cites] Nature. 1997 May 29;387(6632):497-500 [9168111.001]

[Cites] J Psychopharmacol. 1997;11(2):99-106 [9208373.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):14002-8 [9391142.001]

[Cites] Ann N Y Acad Sci. 1998 May 1;840:33-44 [9629234.001]

[Cites] J Neurosci. 1999 Apr 1;19(7):2834-40 [10087094.001]

[Cites] Am J Psychiatry. 1999 Jun;156(6):837-41 [10360120.001]

[Cites] J Neurosci Res. 2004 Dec 1;78(5):702-10 [15505804.001]

[Cites] J Comp Neurol. 2005 Nov 14;492(2):145-77 [16196030.001]

[Cites] Cereb Cortex. 2005 Nov;15(11):1714-22 [15703248.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Nov 22;102(47):17196-201 [16286650.001]

[Cites] Biol Psychiatry. 2006 Feb 1;59(3):244-51 [16140276.001]

[Cites] Neuroscience. 2006 Jun 30;140(2):597-606 [16600515.001]

[Cites] Neuroscience. 2006 Sep 29;142(1):1-20 [16887277.001]

[Cites] Brain Res. 2007 Aug 3;1161:56-64 [17603026.001]

[Cites] Neural Plast. 2007;2007:46276 [18253468.001]

[Cites] Brain Res. 2008 Mar 4;1197:1-12 [18241840.001]

[Cites] Cell Mol Neurobiol. 2008 May;28(3):331-42 [18197473.001]

[Cites] J Neurobiol. 2001 Nov 15;49(3):245-53 [11745662.001]

(PMID = 19180239.001).

[ISSN] 1932-6203

[Journal-full-title] PloS one

[ISO-abbreviation] PLoS ONE

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Gpm6a protein, rat; 0 / Membrane Glycoproteins; 0 / Nerve Tissue Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger

[Other-IDs] NLM/ PMC2629568

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Membrane glycoprotein M6A promotes mu-opioid receptor endocytosis and facilitates receptor sorting into the recycling pathway.

The interaction of mu-opioid receptor (MOPr) with the neuronal membrane glycoprotein M6a is known to facilitate MOPr endocytosis in human embryonic kidney 293 (HEK293) cells.

To further study the role of M6a in the post-endocytotic sorting of MOPr, we investigated the agonist-induced co-internalization of MOPr and M6a and protein targeting after internalization in HEK293 cells that co-expressed HA-tagged MOPr and Myc-tagged M6a.

We found that M6a, MOPr, and Rab 11, a marker for recycling endosomes, co-localized in endocytotic vesicles, indicating that MOPr and M6a are primarily targeted to recycling endosomes after endocytosis.

Furthermore, co-expression of M6a augmented the post-endocytotic sorting of delta-opioid receptors into the recycling pathway, indicating that M6a might have a more general role in opioid receptor post-endocytotic sorting.

The enhanced post-endocytotic sorting of MOPr into the recycling pathway was accompanied by a decrease in agonist-induced receptor down-regulation of M6a in co-expressing cells.

We tested the physiological relevance of these findings in primary cultures of cortical neurons and found that co-expression of M6a markedly increased the translocation of MOPrs from the plasma membrane to intracellular vesicles at steady state and significantly enhanced both constitutive and agonist-induced receptor endocytosis.

In conclusion, our results strongly indicate that M6a modulates MOPr endocytosis and post-endocytotic sorting and has an important role in receptor regulation.

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(PMID = 18574501.001).

[ISSN] 1748-7838

[Journal-full-title] Cell research

[ISO-abbreviation] Cell Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / OPRM1 protein, human; 0 / Receptors, Opioid, mu; EC 2.1.1.- / Methyltransferases; EC 2.1.1.62 / METTL3 protein, human; EC 3.6.1.- / rab GTP-Binding Proteins; EC 3.6.1.- / rab11 protein

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Quorum-sensing regulation of the biofilm matrix genes (pel) of Pseudomonas aeruginosa.

Although QS regulation of swarming and DNA release has been shown to play important roles in biofilm development, regulation of genes directly involved in biosynthesis of biofilm matrix has not been described.

Here, transcription of the pel operon, essential for the production of a glucose-rich matrix exopolysaccharide, is shown to be greatly reduced in lasI and rhlI mutants.

Chemical complementation of the lasI mutant with 3-oxo-dodecanoyl homoserine lactone restores pel transcription to the wild-type level and biofilm formation ability.

These findings thus connect QS signaling and transcription of genes responsible for biofilm matrix biosynthesis.

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[Cites] Biotechniques. 2000 Nov;29(5):948-50, 952 [11084852.001]

[Cites] Mol Microbiol. 2006 Dec;62(5):1264-77 [17059568.001]

[Cites] J Bacteriol. 2001 Nov;183(22):6676-83 [11673439.001]

[Cites] Mol Microbiol. 2004 Feb;51(3):675-90 [14731271.001]

[Cites] J Bacteriol. 2004 May;186(10):2936-45 [15126453.001]

[Cites] Annu Rev Microbiol. 1987;41:435-64 [3318676.001]

[Cites] Science. 1998 Apr 10;280(5361):295-8 [9535661.001]

[Cites] Mol Microbiol. 1998 Sep;29(6):1321-30 [9781871.001]

[Cites] Dev Cell. 2004 Nov;7(5):745-54 [15525535.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Nov 9;101(45):15833-9 [15505212.001]

[Cites] Trends Microbiol. 2005 Jan;13(1):20-6 [15639628.001]

[Cites] Trends Microbiol. 2005 Jan;13(1):27-33 [15639629.001]

[Cites] Microbiology. 2005 Mar;151(Pt 3):985-97 [15758243.001]

[Cites] Environ Microbiol. 2005 Apr;7(4):459-71 [15816912.001]

[Cites] RNA. 2005 Oct;11(10):1579-87 [16131593.001]

[Cites] Mol Microbiol. 2006 Feb;59(4):1114-28 [16430688.001]

[Cites] FEMS Microbiol Rev. 2006 Mar;30(2):274-91 [16472307.001]

[Cites] Int J Med Microbiol. 2006 Apr;296(2-3):73-81 [16476569.001]

[Cites] Cell Microbiol. 2006 Dec;8(12):1841-9 [17026480.001]

[Cites] J Bacteriol. 2001 Oct;183(19):5529-34 [11544214.001]

(PMID = 17496081.001).

[ISSN] 0021-9193

[Journal-full-title] Journal of bacteriology

[ISO-abbreviation] J. Bacteriol.

[Language] ENG

[Grant] United States / NIGMS NIH HHS / GM / R01 GM058213; United States / NIGMS NIH HHS / GM / GM58213

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Bacterial Proteins

[Other-IDs] NLM/ PMC1951888

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Membrane glycoprotein M6a interacts with the micro-opioid receptor and facilitates receptor endocytosis and recycling.

Using a yeast two-hybrid screen, the neuronal membrane glycoprotein M6a, a member of the proteolipid protein family, was identified to be associated with the mu-opioid receptor (MOPr).

Bioluminescence resonance energy transfer and co-immunoprecipitation experiments confirmed that M6a interacts agonist-independently with MOPr in human embryonic kidney 293 cells co-expressing MOPr and M6a.

Co-expression of MOPr with M6a, but not with M6b or DM20, exists in many brain regions, further supporting a specific interaction between MOPr and M6a.

After opioid treatment M6a co-internalizes and then co-recycles with MOPr to cell surface in transfected human embryonic kidney 293 cells.

Moreover, the interaction of M6a and MOPr augments constitutive and agonist-dependent internalization as well as the recycling rate of mu-opioid receptors.

On the other hand, overexpression of a M6a-negative mutant prevents mu-opioid receptor endocytosis, demonstrating an essential role of M6a in receptor internalization.

In addition, we demonstrated the interaction of M6a with a number of other G protein-coupled receptors (GPCRs) such as the delta-opioid receptor, cannabinoid receptor CB1, and somatostatin receptor sst2A, suggesting that M6a might play a general role in the regulation of certain GPCRs.

Taken together, these data provide evidence that M6a may act as a scaffolding molecule in the regulation of GPCR endocytosis and intracellular trafficking.

Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

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(PMID = 17548356.001).

[ISSN] 0021-9258

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Gpm6a protein, rat; 0 / Membrane Glycoproteins; 0 / Nerve Tissue Proteins; 0 / Receptors, Opioid, mu; 0 / Recombinant Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Professor Pel and 'glandular fever'].

[Transliterated title] Professor Pel en 'klierkoorts'.

Pieter Klaesz Pel (1852-1919) was professor of internal medicine at the University of Amsterdam, for more than 35 years.

It is contested whether the patients in question had Hodgkin's disease.

[MeSH-major] Hodgkin Disease / history

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(PMID = 20051175.001).

[ISSN] 1876-8784

[Journal-full-title] Nederlands tijdschrift voor geneeskunde

[ISO-abbreviation] Ned Tijdschr Geneeskd

[Language] dut

[Publication-type] Biography; English Abstract; Historical Article; Journal Article; Portraits

[Publication-country] Netherlands

[Personal-name-as-subject] Pel PK

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] An acute myeloid leukemia M6b blast crisis with giant proerythroblasts in chronic myeloid leukemia.

The case of a 12 yr old female with bcr-abl positive chronic myeloid leukemia who subsequently developed a fatal AML-M6b (pure erythroleukemia) blast crisis is presented.

The case is unique for its rarity of occurrence and for the striking resemblance that the circulating proerythroblasts showed to the giant cells characteristically seen in Parvovirus B19-induced acute pure red cell aplasia.

This is, to the best of our knowledge, the first description of such cells in a blast crisis of chronic myeloid leukemia.

[MeSH-major] Blast Crisis / pathology. Erythroblasts / pathology. Leukemia, Erythroblastic, Acute / pathology. Neoplasms, Multiple Primary / pathology

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(PMID = 19262253.001).

[ISSN] 1536-3678

[Journal-full-title] Journal of pediatric hematology/oncology

[ISO-abbreviation] J. Pediatr. Hematol. Oncol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; X6Q56QN5QC / Hydroxyurea

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] First case of bacteremia due to chromosome-encoded CfxA3-beta-lactamase-producing Capnocytophaga sputigena in a pediatric patient with acute erythroblastic leukemia.

Bacteremia due to Capnocytophaga sputigena occurred in a 4-year and 9-month-old Japanese girl patient with acute erythroblastic leukemia in Shinshu University Hospital, Japan.

The causative Capnocytophaga sputigena isolate was found to be a beta-lactamase-producer demonstrating to possess cfxA3 gene.

The gene responsible for the production of CfxA3-beta-lactamase was proved to be chromosome-encoded, by means of southern hybridization analysis.

[MeSH-major] Bacteremia / microbiology. Capnocytophaga / isolation & purification. Chromosomes, Bacterial. Leukemia, Erythroblastic, Acute / complications. beta-Lactamases / biosynthesis

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(PMID = 18499560.001).

[ISSN] 0949-2321

[Journal-full-title] European journal of medical research

[ISO-abbreviation] Eur. J. Med. Res.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Anti-Bacterial Agents; EC 3.5.2.6 / beta-Lactamases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Glycoprotein M6a is present in glutamatergic axons in adult rat forebrain and cerebellum.

Glycoprotein M6a is a neuronally expressed member of the proteolipid protein (PLP) family of tetraspans.

In vitro studies suggested a potential role in neurite outgrowth and spine formation and previous investigations have identified M6a as a stress-regulated gene.

To investigate whether the distribution of M6a correlates with neuronal structures susceptible to alterations in response to stress, we localized M6a expression in neurons of hippocampal formation, prefrontal cortex and cerebellum using in situ hybridization and confocal immunofluorescence microscopy.

In situ hybridization confirmed that M6a is expressed in dentate gyrus and cerebellar granule neurons and in hippocampal and cortical pyramidal neurons.

Confocal microscopy localized M6a immunoreactivity to distinct sites within axonal membranes, but not in dendrites or neuronal somata.

Moreover, M6a colocalized with synaptic markers of glutamatergic, but not GABAergic nerve terminals.

M6a expression in the adult brain is particularly strong in unmyelinated axonal fibers, i.e. cerebellar parallel and hippocampal mossy fibers.

In contrast, myelinated axons exhibit only minimal M6a immunoreactivity localized exclusively to terminal regions.

The present neuroanatomical data demonstrate that M6a is an axonal component of glutamatergic neurons and that it is localized to distinct sites of the axonal plasma membrane of pyramidal and granule cells.

[MeSH-minor] Animals. Fluorescent Antibody Technique. Gene Expression. Glutamine. In Situ Hybridization. Male. Microscopy, Confocal. RNA, Messenger / analysis. Rats. Rats, Sprague-Dawley. Vesicular Glutamate Transport Proteins / metabolism

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(PMID = 18241840.001).

[ISSN] 0006-8993

[Journal-full-title] Brain research

[ISO-abbreviation] Brain Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger; 0 / Vesicular Glutamate Transport Proteins; 0RH81L854J / Glutamine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Clinicopathological characteristics of erythroblast-rich RAEB and AML M6a in children.

The distinction between RAEB, RAEB-T and AML M6a is difficult when erythroblasts in the bone marrow (BM) exceed 50%.

We analyzed 19 children (2 RAEB, 13 RAEB-T and 4 AML M6a) enrolled in a prospective pathological central review in Japan and divided them into two groups according to the myeloblasts percentage among non-erythroid cells in BM: group A (n = 8), 5-19% myeloblasts; group B (n = 11), 20% or more myeloblasts.

Six with group A and seven with group B treated with AML type chemotherapy achieved complete remission.

Five with group A and seven with group B undergoing SCT are alive at a median of 3 years after diagnosis.

Erythroblast-rich RAEB and AML M6a in children have similar characteristics and may belong to a single disease entity.

[MeSH-major] Anemia, Refractory, with Excess of Blasts / pathology. Erythroblasts / pathology. Granulocyte Precursor Cells / pathology. Leukemia, Myeloid, Acute / pathology

[MeSH-minor] Adolescent. Child. Child, Preschool. Female. Humans. Infant. Japan. Leukocyte Count. Male. Prospective Studies. Remission Induction. Stem Cell Transplantation. Time Factors. Transplantation, Homologous

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[Cites] Pediatr Int. 2005 Oct;47(5):572-4 [16190967.001]

[Cites] Blood. 2006 Jul 15;108(2):419-25 [16609072.001]

[Cites] Leukemia. 2001 Nov;15(11):1713-20 [11681412.001]

[Cites] Br J Haematol. 2003 Jun;121(5):758-67 [12780790.001]

[Cites] Blood. 2001 Sep 15;98(6):1714-20 [11535502.001]

[Cites] Pediatr Blood Cancer. 2007 Jul;49(1):17-22 [16856158.001]

[Cites] Ann Oncol. 1999 Dec;10(12):1419-32 [10643532.001]

[Cites] Br J Haematol. 2002 Apr;117(1):33-9 [11918530.001]

[Cites] Leukemia. 2003 Feb;17(2):277-82 [12592323.001]

[Cites] Leuk Res. 2003 May;27(5):397-404 [12620291.001]

[Cites] Semin Hematol. 1996 Apr;33(2):111-26 [8722682.001]

[Cites] Br J Haematol. 1982 Jun;51(2):189-99 [6952920.001]

[Cites] Am J Clin Pathol. 2005 Aug;124(2):191-8 [16040288.001]

[Cites] Leuk Res. 2002 May;26(5):423-9 [11916513.001]

[Cites] Leukemia. 2002 Aug;16(8):1399-401 [12145675.001]

(PMID = 18951200.001).

[ISSN] 1865-3774

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Journal Article; Multicenter Study

[Publication-country] Japan

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Filopodial protrusions induced by glycoprotein M6a exhibit high motility and aids synapse formation.

M6a is a neuronal membrane glycoprotein whose expression diminishes during chronic stress.

M6a overexpression in rat primary hippocampal neurons induces the formation of filopodial protrusions that could be spine precursors.

As the filopodium and spine motility has been associated with synaptogenesis, we analysed the motility of M6a-induced protrusions by time-lapse imaging.

Our data demonstrate that the motile protrusions formed by the neurons overexpressing M6a were more abundant and moved faster than those formed in control cells.

When different putative M6a phosphorylation sites were mutated, the neurons transfected with a mutant lacking intracellular phosphorylation sites bore filopodia, but these protrusions did not move as fast as those formed by cells overexpressing wild-type M6a.

This suggests a role for M6a phosphorylation state in filopodium motility.

Furthermore, we show that M6a-induced protrusions could be stabilized upon contact with presynaptic region.

The behavior of filopodia from M6a-overexpressing cells and control cells was alike.

Thus, M6a-induced protrusions may be spine precursors that move to reach presynaptic membrane.

We suggest that M6a is a key molecule for spine formation during development.

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(PMID = 20074218.001).

[ISSN] 1460-9568

[Journal-full-title] The European journal of neuroscience

[ISO-abbreviation] Eur. J. Neurosci.

[Language] eng

[Grant] United States / Howard Hughes Medical Institute / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] France

[Chemical-registry-number] 0 / Gpm6a protein, rat; 0 / Membrane Glycoproteins; 0 / Nerve Tissue Proteins; 0 / Recombinant Fusion Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Membrane glycoprotein M6B interacts with the human serotonin transporter.

In the present study, using the yeast two-hybrid system, we identified the membrane glycoprotein M6B as a binding partner of SERT.

M6B belongs to a proteolipid protein family, which is expressed in neurons and in oligodendrocytes in the brain.

The co-expression of SERT with M6B results in a significant decrease in SERT-mediated serotonin uptake caused by a down-regulation of SERT surface expression.

Furthermore, we find, using confocal microscopy, that M6B co-localizes with SERT when transiently expressed in HEK-MSR-293 cells and when endogenously expressed in RN46A cells.

Taken together, our data suggest that M6B regulates the serotonin uptake by affecting cellular trafficking of the serotonin transporter.

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[Cites] Science. 1999 Jul 30;285(5428):763-6 [10427004.001]

[Cites] Brain Res Mol Brain Res. 1999 Jul 23;71(1):120-6 [10407194.001]

[Cites] J Neurosci Res. 2000 Oct 1;62(1):1-8 [11002282.001]

[Cites] Proc Natl Acad Sci U S A. 1993 Mar 15;90(6):2542-6 [7681602.001]

[Cites] Proc Natl Acad Sci U S A. 2007 May 8;104(19):8119-24 [17452640.001]

[Cites] Int J Dev Neurosci. 1997 Jun;15(3):285-93 [9253653.001]

[Cites] Mol Cell Neurosci. 2001 Dec;18(6):593-605 [11749036.001]

[Cites] Mol Interv. 2004 Apr;4(2):109-23 [15087484.001]

[Cites] Neuron. 2003 Oct 30;40(3):537-49 [14642278.001]

[Cites] Curr Drug Targets. 2006 Dec;7(12):1659-69 [17168841.001]

[Cites] J Neurosci. 1997 Jan 1;17(1):45-57 [8987735.001]

[Cites] Science. 1991 Oct 25;254(5031):579-80 [1948036.001]

[Cites] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5665-9 [2441390.001]

[Cites] Nature. 1991 Nov 7;354(6348):66-70 [1944572.001]

[Cites] J Psychopharmacol. 1998;12(2):115-21 [9694022.001]

[Cites] Prog Neuropsychopharmacol Biol Psychiatry. 2005 Feb;29(2):297-303 [15694238.001]

[Cites] Biol Psychiatry. 1990 Sep 1;28(5):443-54 [2207221.001]

[Cites] Biochemistry. 2005 Oct 18;44(41):13612-24 [16216085.001]

[Cites] J Cell Biol. 2002 Apr 15;157(2):327-36 [11956232.001]

[Cites] Biochem Soc Trans. 2001 Nov;29(Pt 6):722-8 [11709063.001]

[Cites] J Biol Chem. 2007 Jul 27;282(30):22239-47 [17548356.001]

[Cites] Biochim Biophys Acta. 1993 Oct 4;1144(3):249-63 [8104483.001]

[Cites] Eur J Pharmacol. 1999 Mar 5;368(2-3):277-83 [10193665.001]

[Cites] J Neurosci Res. 1998 Jun 15;52(6):633-40 [9669312.001]

[Cites] Nature. 2005 Sep 8;437(7056):215-23 [16041361.001]

[Cites] Trends Neurosci. 1992 Jul;15(7):265-8 [1381123.001]

[Cites] FEBS Lett. 2004 May 7;565(1-3):1-5 [15135042.001]

[Cites] J Biol Chem. 2006 Sep 29;281(39):28901-9 [16870614.001]

[Cites] Eur J Neurosci. 2006 Dec;24(11):3141-52 [17156375.001]

[Cites] J Neurochem. 2006 Apr;97 Suppl 1:3-10 [16635244.001]

[Cites] J Biol Chem. 2004 Sep 10;279(37):38770-8 [15226315.001]

[Cites] J Comp Neurol. 1996 Jul 8;370(4):465-78 [8807448.001]

[Cites] J Am Chem Soc. 2008 Mar 26;130(12):3853-65 [18314975.001]

[Cites] J Neurobiol. 1996 Feb;29(2):138-50 [8821173.001]

[Cites] Eur J Neurosci. 2006 Jul;24(1):55-64 [16882008.001]

[Cites] Am J Med Genet A. 2004 Jul 15;128A(2):156-8 [15214007.001]

(PMID = 18581270.001).

[ISSN] 0895-8696

[Journal-full-title] Journal of molecular neuroscience : MN

[ISO-abbreviation] J. Mol. Neurosci.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / GPM6A protein, human; 0 / GPM6B protein, human; 0 / Membrane Glycoproteins; 0 / Nerve Tissue Proteins; 0 / Serotonin Plasma Membrane Transport Proteins; 333DO1RDJY / Serotonin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

: e14592 Background: During the process of malignant transformation, the tumor cell adopts a new form of metabolism, characterized by aerobic glycolysis and altered TCA cycle flux, that enable it to meet the energetic and biosynthetic demands of proliferation.

METHODS: We have characterized the proliferative and metabolic effects of phenformin, a member of the biguanide family of compounds used in the treatment of diabetes, on the bcr-abl expressing K562 erythroleukemia cell line, and compared the resulting phenotype to those of imatinib and rapamycin, two targeted agents used in the treatment of malignant disease.

Phenformin treatment eliminated the mitochondrial contribution to anabolic metabolism, through inhibition of Complex I of the Electron Transport Chain, as demonstrated by reduced oxygen consumption and intracellular ATP levels.

CONCLUSIONS: Our results confirm the importance of metabolism to the proliferation of malignant cells, thereby validating anabolic metabolism's potential for therapeutic intervention.

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(PMID = 27963742.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Characterization of AZD8931, a potent reversible small molecule inhibitor against epidermal growth factor receptor (EGFR), erythroblastic leukemia viral oncogene homolog 2 (HER2) and 3 (HER3) with a unique and balanced pharmacological profile.

Characterization of a novel tyrosine kinase inhibitor with a potent and balanced profile against EGFR, HER2 (erbB2), and HER3 (erbB3) has been carried out.

These assays have provided unique insights into the pharmacology of these drugs that result from the varying levels of HER and their associated ligands.

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(PMID = 27963188.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

: Effective gene therapy for β-thalassemia major (β-TM) requires consistent, high expression of human β-globin (hβ-globin) in red blood cells (RBCs).

Several groups have now shown that lentiviral (LV) vectors stably transmit the hβ/hγ-globin genes and large elements of the locus control region, resulting in correction of the murine thalassemia intermedia (TI) phenotype and survival of mice with the TM phenotype.

We observed a consistent twofold-higher hβ expression from insulated vectors in single-copy mouse erythroleukemia cell clones, an increase that resulted from reduced position effect variegation (PEV) and increased probability of expression from individual integrants.

These studies have important implications for vector design for clinical trials for gene therapy for hemoglobinopathies.

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[Copyright] Copyright © 2007 The American Society of Gene Therapy. Published by Elsevier Inc. All rights reserved.

(PMID = 28182916.001).

[ISSN] 1525-0024

[Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy

[ISO-abbreviation] Mol. Ther.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Developmental expression and molecular analysis of two Meloidogyne incognita pectate lyase genes.

Two cDNAs (designated Mi-pel-1 and Mi-pel-2) encoding pectate lyases were isolated from the root-knot nematode, Meloidogyne incognita, oesophageal gland-cell subtractive cDNA libraries, and the corresponding genomic DNAs were subsequently cloned.

Southern blot analyses revealed that homologues to these pectate lyase genes were broadly distributed in Meloidogyne species, and present as members of a small multigene family.

Mi-pel-1 and Mi-pel-2 encoded, respectively, predicted proteins of 271 and 280 amino acids, each of which was preceded by a signal peptide for secretion.

Interestingly, these pectate lyases showed diversity at the amino acid level, with only 31% identity and 49% similarity.

These pectate lyases were classified into the same family of pectate lyases with those of other phytoparasitic nematodes that contain four conserved regions characteristic of the class III pectate lyases of microbes.

In situ mRNA hybridisation analyses showed the transcripts of Mi-pel-1 and Mi-pel-2 accumulated exclusively within the subventral oesophageal gland cells of M. incognita.

These results indicated that these pectate lyases, like cellulases, could be secreted into plant tissues to facilitate the penetration and intercellular migration of M. incognita during the early stages of plant parasitism.

[MeSH-major] Gene Expression Regulation, Developmental / genetics. Polysaccharide-Lyases / genetics. Tylenchoidea / genetics

[MeSH-minor] Amino Acid Sequence. Animals. Base Sequence. Blotting, Southern / methods. Cloning, Molecular / methods. DNA, Circular / genetics. DNA, Helminth / genetics. Genes, Helminth / genetics. In Situ Hybridization / methods. Molecular Sequence Data. Phylogeny. Reverse Transcriptase Polymerase Chain Reaction / methods

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(PMID = 15862581.001).

[ISSN] 0020-7519

[Journal-full-title] International journal for parasitology

[ISO-abbreviation] Int. J. Parasitol.

[Language] eng

[Databank-accession-numbers] GENBANK/ AF527788/ AY327873/ AY515702/ AY515703

[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 / DNA, Circular; 0 / DNA, Helminth; EC 4.2.2.- / Polysaccharide-Lyases; EC 4.2.2.2 / pectate lyase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] PEL, Kaposi's sarcoma HHV8+ and idiopathic T-lymphocitopenia CD4+.

We described a case report of a 36-year-old woman with a 10-year-history of idiopathic CD4+ T-lymphocitopenia and Kaposi's sarcoma HHV8+ who developed recurrent pleural effusion.

Laboratory and instrumental tests with morphologic, immunophenotypic and molecular analysis of pleural sediment suggest us the diagnosis of primary effusion lymphoma (PEL).

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(PMID = 17566517.001).

[ISSN] 0009-9074

[Journal-full-title] La Clinica terapeutica

[ISO-abbreviation] Clin Ter

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The stress-regulated protein M6a is a key modulator for neurite outgrowth and filopodium/spine formation.

We have recently identified the glycoprotein M6a as a stress-responsive gene in the hippocampal formation.

This gene is down-regulated in the hippocampus of both socially and physically stressed animals, and this effect can be reversed by antidepressant treatment.

In the present work, we analyzed the biological function of the M6a protein.

Immunohistochemistry showed that the M6a protein is abundant in all hippocampal subregions, and subcellular analysis in primary hippocampal neurons revealed its presence in membrane protrusions (filopodia/spines).

Transfection experiments revealed that M6a overexpression induces neurite formation and increases filopodia density in hippocampal neurons.

M6a knockdown with small interference RNA methodology showed that M6a low-expressing neurons display decreased filopodia number and a lower density of synaptophysin clusters.

Taken together, our findings indicate that M6a plays an important role in neurite/filopodium outgrowth and synapse formation.

Therefore, reduced M6a expression might be responsible for the morphological alterations found in the hippocampus of chronically stressed animals.

Potential mechanisms that might explain the biological effects of M6a are discussed.

Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

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[Cites] Neuron. 1996 Jul;17(1):91-102 [8755481.001]

[Cites] J Neurosci. 1996 May 15;16(10):3534-40 [8627386.001]

[Cites] Science. 1998 Jan 23;279(5350):509-14 [9438836.001]

[Cites] Psychopharmacology (Berl). 1997 Dec;134(4):319-29 [9452163.001]

[Cites] J Neurosci. 1998 Nov 1;18(21):8900-11 [9786995.001]

[Cites] Annu Rev Neurosci. 1999;22:105-22 [10202533.001]

[Cites] Am J Psychiatry. 1999 Jun;156(6):837-41 [10360120.001]

[Cites] J Cell Biol. 1999 Jun 14;145(6):1265-75 [10366598.001]

[Cites] J Neurocytol. 1998 Sep;27(9):695-703 [10447243.001]

[Cites] Prog Brain Res. 2005;147:29-37 [15581695.001]

[Cites] Neuroscience. 2005;131(1):43-54 [15680690.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Nov 9;96(23):13438-43 [10557339.001]

[Cites] Neuroscience. 2000;97(2):253-66 [10799757.001]

[Cites] Brain Res. 2000 Oct 13;880(1-2):147-58 [11032999.001]

[Cites] Biol Psychiatry. 2000 Oct 15;48(8):721-31 [11063969.001]

[Cites] Hippocampus. 2000;10(5):582-6 [11075828.001]

[Cites] Nat Rev Neurosci. 2000 Dec;1(3):173-80 [11257905.001]

[Cites] J Neurosci. 2001 Jul 15;21(14):5169-81 [11438592.001]

[Cites] J Neurosci. 2001 Aug 15;21(16):6105-14 [11487634.001]

[Cites] J Neurosci. 2001 Aug 15;21(16):6292-7 [11487652.001]

[Cites] Pharmacol Biochem Behav. 2002 Aug;73(1):247-58 [12076743.001]

[Cites] J Neurosci. 2002 Sep 1;22(17):7398-407 [12196561.001]

[Cites] Biochem Biophys Res Commun. 2002 Oct 4;297(4):722-8 [12359212.001]

[Cites] Annu Rev Cell Dev Biol. 2002;18:601-35 [12142283.001]

[Cites] Hippocampus. 2002;12(5):585-91 [12440574.001]

[Cites] J Neurosci. 2003 Jan 15;23(2):659-65 [12533625.001]

[Cites] Neuron. 2003 Jan 23;37(2):263-74 [12546821.001]

[Cites] Eur J Neurosci. 2003 Jun;17(11):2447-56 [12814376.001]

[Cites] Rev Neurosci. 2003;14(3):233-40 [14513866.001]

[Cites] Neuron. 2003 Oct 9;40(2):243-64 [14556707.001]

[Cites] J Neurosci Res. 2003 Dec 1;74(5):744-53 [14635225.001]

[Cites] Eur J Neurosci. 2004 Feb;19(3):659-66 [14984416.001]

[Cites] Curr Opin Pharmacol. 2004 Feb;4(1):58-64 [15018840.001]

[Cites] Neuron. 2004 Oct 14;44(2):321-34 [15473970.001]

[Cites] Nature. 2004 Oct 14;431(7010):782-8 [15483599.001]

[Cites] J Neurosci. 1991 Jun;11(6):1617-26 [1904480.001]

[Cites] J Neurobiol. 1992 Feb;23(1):71-88 [1564456.001]

[Cites] Brain Res. 1992 Aug 21;588(2):341-5 [1393587.001]

[Cites] Neuron. 1993 Sep;11(3):423-31 [8398137.001]

[Cites] Arch Gen Psychiatry. 1997 Jul;54(7):597-606 [9236543.001]

(PMID = 16286650.001).

[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 / Gpm6a protein, rat; 0 / Membrane Glycoproteins; 0 / Nerve Tissue Proteins; 0 / RNA, Small Interfering

[Other-IDs] NLM/ PMC1287971

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Connecting quorum sensing, c-di-GMP, pel polysaccharide, and biofilm formation in Pseudomonas aeruginosa through tyrosine phosphatase TpbA (PA3885).

This screen identified the PA3885 mutant, which had 147-fold more biofilm than the wild-type strain.

Whole transcriptome analysis showed that loss of PA3885 activated expression of the pel locus, an operon that encodes for the synthesis of extracellular matrix polysaccharide.

Genetic screening identified that loss of PelABDEG and the PA1120 protein (which contains a GGDEF-motif) suppressed the phenotypes of the PA3885 mutant, suggesting that the function of the PA3885 protein is to regulate 3,5-cyclic diguanylic acid (c-di-GMP) concentrations as a phosphatase since c-di-GMP enhances biofilm formation by activating PelD, and c-di-GMP inhibits swarming.

Loss of PA3885 protein increased cellular c-di-GMP concentrations; hence, PA3885 protein is a negative regulator of c-di-GMP production.

Las-mediated quorum sensing positively regulates expression of the PA3885 gene.

These results show that the PA3885 protein responds to AHL signals and likely dephosphorylates PA1120, which leads to reduced c-di-GMP production.

This inhibits matrix exopolysaccharide formation, which leads to reduced biofilm formation; hence, we provide a mechanism for quorum sensing control of biofilm formation through the pel locus and suggest PA3885 should be named TpbA for tyrosine phosphatase related to biofilm formation and PA1120 should be TpbB.

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[Cites] J Bacteriol. 2007 Nov;189(22):8154-64 [17586642.001]

[Cites] Curr Opin Microbiol. 2007 Dec;10(6):644-8 [17981495.001]

[Cites] J Bacteriol. 2008 Apr;190(8):2671-9 [18245294.001]

[Cites] J Biol Chem. 2008 Apr 11;283(15):9933-44 [18256026.001]

[Cites] Appl Microbiol Biotechnol. 2008 Jul;79(5):843-58 [18481058.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Nov 23;96(24):13904-9 [10570171.001]

[Cites] Nature. 2000 Aug 31;406(6799):959-64 [10984043.001]

[Cites] J Bacteriol. 2000 Nov;182(21):5990-6 [11029417.001]

[Cites] Trends Microbiol. 2000 Nov;8(11):498-504 [11121759.001]

[Cites] Mol Microbiol. 2002 Feb;43(3):809-21 [11929534.001]

[Cites] Clin Microbiol Rev. 2002 Apr;15(2):155-66 [11932228.001]

[Cites] Mol Microbiol. 2002 Oct;46(2):571-86 [12406230.001]

[Cites] J Bacteriol. 2003 Feb;185(3):1027-36 [12533479.001]

[Cites] J Bacteriol. 2003 Apr;185(7):2080-95 [12644477.001]

[Cites] J Biol Chem. 2003 Apr 18;278(16):13627-32 [12556522.001]

[Cites] J Biol Chem. 2003 Apr 18;278(16):14429-41 [12562757.001]

[Cites] Mol Microbiol. 2004 Feb;51(3):675-90 [14731271.001]

[Cites] Arch Microbiol. 2004 Mar;181(3):171-81 [14745484.001]

[Cites] Appl Microbiol Biotechnol. 2004 May;64(4):515-24 [14727089.001]

[Cites] J Bacteriol. 2004 Jul;186(14):4466-75 [15231778.001]

[Cites] Mol Microbiol. 2004 Aug;53(4):1075-87 [15306012.001]

[Cites] Proc Natl Acad Sci U S A. 1979 Apr;76(4):1648-52 [377280.001]

[Cites] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7347-51 [7012838.001]

[Cites] J Bacteriol. 1986 Mar;165(3):1002-10 [3005231.001]

[Cites] J Biol Chem. 1990 Nov 5;265(31):18933-43 [2172238.001]

[Cites] Methods Enzymol. 1991;201:477-82 [1943774.001]

[Cites] Science. 1993 May 21;260(5111):1127-30 [8493556.001]

[Cites] Annu Rev Microbiol. 1993;47:597-626 [8257110.001]

[Cites] J Bacteriol. 1995 Feb;177(3):654-9 [7836299.001]

[Cites] Proc Natl Acad Sci U S A. 1995 Jun 20;92(13):5910-4 [7597052.001]

[Cites] Proc Natl Acad Sci U S A. 1995 Jul 3;92(14):6424-8 [7604006.001]

[Cites] Mol Microbiol. 2008 Jul;69(2):376-89 [18485075.001]

[Cites] Mol Microbiol. 2008 Sep;69(5):1153-64 [18573179.001]

[Cites] J Mol Biol. 2008 Nov 7;383(2):414-23 [18775435.001]

[Cites] Trends Microbiol. 2008 Oct;16(10):496-506 [18775660.001]

[Cites] J Bacteriol. 2009 Jan;191(1):169-77 [18952786.001]

[Cites] Microb Biotechnol. 2009 Jan;2(1):62-74 [21261882.001]

[Cites] Proteins. 1991;11(2):95-110 [1946347.001]

[Cites] Biochem J. 1995 Nov 1;311 ( Pt 3):921-7 [7487952.001]

[Cites] J Biochem. 1996 Dec;120(6):1055-63 [9010748.001]

[Cites] J Bacteriol. 1997 May;179(10):3127-32 [9150205.001]

[Cites] Science. 1998 Apr 10;280(5361):295-8 [9535661.001]

[Cites] Bioinformatics. 1998;14(4):378-9 [9632836.001]

[Cites] Annu Rev Biophys Biomol Struct. 1998;27:133-64 [9646865.001]

[Cites] Mol Microbiol. 1998 Oct;30(2):285-93 [9791174.001]

[Cites] Mol Microbiol. 1998 Oct;30(2):295-304 [9791175.001]

[Cites] J Bacteriol. 1998 Dec;180(23):6384-8 [9829950.001]

[Cites] Biotechnol Bioeng. 2004 Dec 5;88(5):630-42 [15470704.001]

[Cites] Mol Microbiol. 2005 Jan;55(2):368-80 [15659157.001]

[Cites] Infect Immun. 2005 Apr;73(4):1954-63 [15784535.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Oct 4;102(40):14422-7 [16186483.001]

[Cites] J Microbiol. 2005 Oct;43(5):443-50 [16273037.001]

[Cites] J Bacteriol. 2006 Jan;188(1):305-16 [16352847.001]

[Cites] J Mol Microbiol Biotechnol. 2005;9(3-4):125-31 [16415586.001]

[Cites] Int J Med Microbiol. 2006 Apr;296(2-3):83-91 [16483840.001]

[Cites] J Biol Chem. 2006 Mar 24;281(12):8090-9 [16418169.001]

[Cites] Curr Opin Microbiol. 2006 Apr;9(2):218-28 [16530465.001]

[Cites] Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2833-8 [16477005.001]

[Cites] Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2839-44 [16477007.001]

[Cites] Microbiology. 2006 Jun;152(Pt 6):1679-86 [16735731.001]

[Cites] DNA Res. 2005;12(5):291-9 [16769691.001]

[Cites] Appl Environ Microbiol. 2006 Jul;72(7):5027-36 [16820502.001]

[Cites] J Bacteriol. 2007 May;189(9):3603-12 [17337585.001]

[Cites] J Bacteriol. 2007 Jul;189(14):5383-6 [17496081.001]

[Cites] Nat Cell Biol. 2007 Jul;9(7):797-803 [17558395.001]

[Cites] J Bacteriol. 2007 Sep;189(18):6695-703 [17631636.001]

[Cites] Environ Microbiol. 2007 Oct;9(10):2475-85 [17803773.001]

[Cites] Mol Microbiol. 2007 Sep;65(6):1474-84 [17824927.001]

[Cites] J Bacteriol. 2007 Nov;189(22):8165-78 [17586641.001]

(PMID = 19543378.001).

[ISSN] 1553-7374

[Journal-full-title] PLoS pathogens

[ISO-abbreviation] PLoS Pathog.

[Language] ENG

[Grant] United States / NIBIB NIH HHS / EB / R01 EB003872

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Adhesins, Bacterial; 0 / Bacterial Proteins; 0 / Glycolipids; 0 / Polysaccharides, Bacterial; 0 / rhamnolipid; 42HK56048U / Tyrosine; 61093-23-0 / bis(3',5')-cyclic diguanylic acid; EC 3.1.3.48 / Protein Tyrosine Phosphatases; H2D2X058MU / Cyclic GMP

[Other-IDs] NLM/ PMC2691606

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Rapamycin is efficacious against primary effusion lymphoma (PEL) cell lines in vivo by inhibiting autocrine signaling.

Primary effusion lymphoma (PEL) appears as an AIDS-defining lymphoma and like Kaposi sarcoma has been linked to Kaposi sarcoma-associated herpesvirus (KSHV).

We find that (1) rapamycin is efficacious against PEL in culture and in a murine xenograft model;.

(2) mTOR, its activator Akt, and its target p70S6 kinase are phosphorylated in PEL;.

This validates sirolimus as a new treatment option for PEL.

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[Cites] Am J Surg Pathol. 1999 Nov;23(11):1393-400 [10555008.001]

[Cites] Cancer Res. 2004 Jul 15;64(14):4790-9 [15256448.001]

[Cites] Nature. 1999 Dec 23-30;402(6764):889-94 [10622254.001]

[Cites] J Infect Dis. 2000 Dec;182(6):1809-10 [11069261.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Jan 2;98(1):136-41 [11134523.001]

[Cites] Clin Infect Dis. 2001 May 15;32(10):1502-5 [11317254.001]

[Cites] Clin Cancer Res. 2001 Jun;7(6):1758-64 [11410517.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10320-5 [11504907.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10314-9 [11504908.001]

[Cites] Cancer. 2001 Dec 15;92(12):3076-84 [11753987.001]

[Cites] J Infect. 2001 Oct;43(3):195-9 [11798259.001]

[Cites] J Biol Chem. 2002 Apr 19;277(16):13907-17 [11847216.001]

[Cites] J Virol. 2002 Jun;76(12):6213-23 [12021355.001]

[Cites] Clin Microbiol Rev. 2002 Jul;15(3):439-64 [12097251.001]

[Cites] Science. 2002 Nov 15;298(5597):1432-5 [12434062.001]

[Cites] Cancer Res. 2002 Dec 15;62(24):7291-7 [12499272.001]

[Cites] J Virol. 2003 May;77(10):5759-73 [12719569.001]

[Cites] Nat Med. 2003 May;9(5):554-61 [12692543.001]

[Cites] Cancer Res. 2003 May 1;63(9):2010-5 [12727810.001]

[Cites] Blood. 2003 May 15;101(10):4115-21 [12531789.001]

[Cites] Cancer Res. 2003 Aug 1;63(15):4472-80 [12907620.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Sep 2;100(18):10399-404 [12925741.001]

[Cites] Cancer Cell. 2003 Nov;4(5):343-8 [14667501.001]

[Cites] J Virol. 2004 Feb;78(4):1918-27 [14747556.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4821-6 [15047889.001]

[Cites] Nat Med. 2004 Jun;10(6):594-601 [15156201.001]

[Cites] Nat Rev Microbiol. 2004 Aug;2(8):656-68 [15263900.001]

[Cites] Methods Mol Biol. 2005;292:449-80 [15507725.001]

[Cites] Cancer Res. 1988 Feb 1;48(3):589-601 [3335022.001]

[Cites] Science. 1994 Dec 16;266(5192):1865-9 [7997879.001]

[Cites] Blood. 1995 Aug 15;86(4):1276-80 [7632932.001]

[Cites] Lancet. 1995 Sep 23;346(8978):799-802 [7674745.001]

[Cites] Nat Med. 1995 Dec;1(12):1274-8 [7489408.001]

[Cites] J Exp Med. 1996 May 1;183(5):2385-90 [8642350.001]

[Cites] Blood. 1996 Oct 1;88(7):2648-54 [8839859.001]

[Cites] J Acquir Immune Defic Syndr Hum Retrovirol. 1996 Nov 1;13(3):215-26 [8898666.001]

[Cites] J Virol. 1997 Jan;71(1):715-9 [8985403.001]

[Cites] Blood. 1998 Apr 1;91(7):2475-81 [9516148.001]

[Cites] J Exp Med. 1998 Jul 20;188(2):405-8 [9670053.001]

[Cites] N Engl J Med. 1998 Aug 13;339(7):444-9 [9700178.001]

[Cites] J Virol. 1998 Oct;72(10):8309-15 [9733875.001]

[Cites] N Engl J Med. 1998 Nov 5;339(19):1358-63 [9801396.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4546-51 [10200299.001]

[Cites] Leukemia. 1999 Apr;13(4):634-40 [10214873.001]

[Cites] Transplantation. 1999 Apr 27;67(8):1200-1 [10232577.001]

[Cites] Transplantation. 1999 May 15;67(9):1236-42 [10342315.001]

[Cites] Blood. 1999 Jun 15;93(12):4034-43 [10361100.001]

[Cites] J Virol. 1999 Jul;73(7):6136-40 [10364372.001]

[Cites] Blood. 1999 Oct 15;94(8):2871-9 [10515891.001]

[Cites] Nat Cell Biol. 2004 Nov;6(11):1122-8 [15467718.001]

[Cites] Trends Biochem Sci. 2005 Jan;30(1):35-42 [15653324.001]

[Cites] Science. 2005 Feb 18;307(5712):1098-101 [15718470.001]

[Cites] N Engl J Med. 2005 Mar 31;352(13):1317-23 [15800227.001]

[Cites] Clin Cancer Res. 2005 Apr 15;11(8):3102-8 [15837766.001]

[Cites] AIDS Rev. 2005 Jan-Mar;7(1):56-61 [15875661.001]

[Cites] Cancer Res. 2005 Sep 1;65(17):7800-8 [16140948.001]

[Cites] Cancer Cell. 2005 Sep;8(3):179-83 [16169463.001]

[Cites] Cancer Res. 2006 Jan 1;66(1):168-74 [16397229.001]

[Cites] Cancer Res. 2006 Apr 1;66(7):3658-66 [16585191.001]

[Cites] Nat Genet. 2004 Jul;36(7):683-5 [15220917.001]

[Cites] Nat Genet. 2004 Jul;36(7):687-93 [15220918.001]

[Cites] Eur Cytokine Netw. 1999 Dec;10(4):501-8 [10586116.001]

(PMID = 17082322.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / HL083469; United States / NCI NIH HHS / CA / R01 CA109232; United States / NCI NIH HHS / CA / R01 CA163217; United States / NIDCR NIH HHS / DE / R01 DE018304-02; United States / NCI NIH HHS / CA / CA096500; United States / NIDCR NIH HHS / DE / DE018304-01; United States / NIDCR NIH HHS / DE / R01 DE018304; United States / NIAID NIH HHS / AI / AI057157; United States / NIDCR NIH HHS / DE / R01 DE018304-01; United States / NCI NIH HHS / CA / CA098110; United States / NCI NIH HHS / CA / CA109232; United States / NCI NIH HHS / CA / CA112935; United States / NIDCR NIH HHS / DE / R01 DE018304-03; United States / NIDCR NIH HHS / DE / DE018304-02; United States / NCI NIH HHS / CA / R01 CA098110; United States / NHLBI NIH HHS / HL / R01 HL083469; United States / NIDCR NIH HHS / DE / DE018304-03; United States / NIAID NIH HHS / AI / U54 AI057157; United States / NCI NIH HHS / CA / R01 CA096500

[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 / Cytokines; 0 / RNA, Messenger; W36ZG6FT64 / Sirolimus

[Other-IDs] NLM/ PMC1801055

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The pel genes of the Pseudomonas aeruginosa PAK strain are involved at early and late stages of biofilm formation.

Biofilm-deficient P. aeruginosa PAK strains affected in a seven-gene cluster called pel were characterized.

The pel genes encode proteins with similarity to components involved in polysaccharide biogenesis, of which PelF is a putative glycosyltransferase.

The pel genes were previously identified in the P. aeruginosa PA14 strain as required for the production of a glucose-rich matrix material involved in the formation of a thick pellicle and resistant biofilm.

However, in PA14, the pel mutants have no clear phenotype in the initiation phase of attachment.

It was shown that pel mutations in the PAK strain had little influence on biofilm initiation but, as in PA14, appeared to generate the least robust and mature biofilms.

Strikingly, by constructing pel mutants in a non-piliated P. aeruginosa PAK strain, an unexpected effect of the pel mutation in the early phase of biofilm formation was discovered, since it was observed that these mutants were severely defective in the attachment process on solid surfaces.

The pel gene cluster is conserved in other Gram-negative bacteria, and mutation in a Ralstonia solanacearum pelG homologue, ragG, led to an adherence defect.

[MeSH-minor] Bacterial Adhesion. Culture Media. DNA Transposable Elements. Gene Expression Regulation, Bacterial. Glycosyltransferases / genetics. Glycosyltransferases / metabolism. Hydrophobic and Hydrophilic Interactions. Multigene Family. Mutation. Polysaccharides, Bacterial / genetics. Polysaccharides, Bacterial / metabolism

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(PMID = 15758243.001).

[ISSN] 1350-0872

[Journal-full-title] Microbiology (Reading, England)

[ISO-abbreviation] Microbiology (Reading, Engl.)

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Bacterial Proteins; 0 / Culture Media; 0 / DNA Transposable Elements; 0 / Polysaccharides, Bacterial; EC 2.4.- / Glycosyltransferases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A colorimetric sensor array for identification of toxic gases below permissible exposure limits.

A colorimetric sensor array has been developed for the rapid and sensitive detection of 20 toxic industrial chemicals (TICs) at their PELs (permissible exposure limits).

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[Cites] Nat Mater. 2003 Jan;2(1):19-24 [12652667.001]

[Cites] Nature. 2000 Aug 17;406(6797):710-3 [10963592.001]

[Cites] Anal Chem. 2009 Aug 1;81(15):6526-33 [20337402.001]

[Cites] Anal Chem. 2009 Jul 1;81(13):5281-90 [19563211.001]

[Cites] Org Lett. 2008 Oct 16;10(20):4405-8 [18783231.001]

[Cites] Nat Chem. 2009 Oct;1(7):562-7 [20160982.001]

[Cites] Anal Chem. 2006 Jun 1;78(11):3591-600 [16737212.001]

[Cites] Angew Chem Int Ed Engl. 2005 Jul 18;44(29):4528-32 [16003792.001]

[Cites] MRS Bull. 2004 Oct;29(10):720-5 [15991401.001]

[Cites] Acc Chem Res. 2004 Sep;37(9):663-72 [15379582.001]

[Cites] J Org Chem. 2007 Feb 2;72(3):687-99 [17253783.001]

(PMID = 20221484.001).

[ISSN] 1364-548X

[Journal-full-title] Chemical communications (Cambridge, England)

[ISO-abbreviation] Chem. Commun. (Camb.)

[Language] ENG

[Grant] United States / NIEHS NIH HHS / ES / U01 ES016011; United States / NIEHS NIH HHS / ES / U01 ES016011-04; United States / NIEHS NIH HHS / ES / U01ES016011

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] England

[Chemical-registry-number] 0 / Gases

[Other-IDs] NLM/ NIHMS229286; NLM/ PMC2976522

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Leukotriene A4 hydrolase expression in PEL cells is regulated at the transcriptional level and leads to increased leukotriene B4 production.

Primary effusion lymphoma (PEL) is a herpesvirus-8-associated lymphoproliferative disease characterized by migration of tumor cells to serous body cavities.

PEL cells originate from postgerminal center B cells and share a remarkable alteration in B cell transcription factor expression and/or activation with classical Hodgkin's disease cells.

Comparative analysis of gene expression by cDNA microarray of BCBL-1 cells (PEL), L-428 (classical Hodgkin's disease), and BJAB cells revealed a subset of genes that were differentially expressed in BCBL-1 cells.

Among these, four genes involved in cell migration and chemotaxis were strongly up-regulated in PEL cells: leukotriene A4 (LTA4) hydrolase (LTA4H), IL-16, thrombospondin-1 (TSP-1), and selectin-P ligand (PSGL-1).

Up-regulation of LTA4H was investigated at the transcriptional level.

Formation of a specific DNA-protein complex in this region was confirmed by EMSA.

[MeSH-minor] Cell Line, Tumor. Enzyme Activation / genetics. Gene Expression Profiling. Hodgkin Disease / genetics. Humans. Inflammation / genetics. Inflammation / immunology. Interleukin-16 / physiology. Membrane Glycoproteins / biosynthesis. Membrane Glycoproteins / genetics. Membrane Glycoproteins / physiology. Promoter Regions, Genetic. RNA, Messenger / biosynthesis. Thrombospondin 1 / biosynthesis. Thrombospondin 1 / genetics. Thrombospondin 1 / physiology. Transcription, Genetic

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(PMID = 16709867.001).

[ISSN] 0022-1767

[Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)

[ISO-abbreviation] J. Immunol.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Interleukin-16; 0 / Membrane Glycoproteins; 0 / P-selectin ligand protein; 0 / RNA, Messenger; 0 / Thrombospondin 1; 1HGW4DR56D / Leukotriene B4; EC 3.3.2.- / Epoxide Hydrolases; EC 3.3.2.- / leukotriene A4 hydrolase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] KSHV-infected PEL cell lines exhibit a distinct gene expression profile.

We analyzed the gene expression profiles of lymphocyte-originated tumor cell lines - primary effusion lymphoma (PEL) cell lines, T-cell leukemia (TCL) cell lines, Burkitt lymphoma (BL) cell lines - and two sets of normal peripheral blood mononuclear cells (PBMCs) - in order to determine characteristic gene expression profiles for each of the former three groups.

And we found that these cell lines showed respective typical gene expression profiles and classified into clear four groups, PEL, TCL, BL, and normal PBMCs.

Two B lymphocyte-originated tumor cell lines, PEL and BL cell lines, clearly exhibited distinct gene expression profiles, respectively.

Even though there was only one line that was co-infected with both Kaposi's sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV), KSHV seemed to govern the gene expression profile of the co-infected line.

These data suggested not only that established typical tumor cell lines show a distinct gene expression profile but also that this profile may be governed by certain viruses.

[MeSH-major] Gene Expression Regulation, Neoplastic. Gene Expression Regulation, Viral. Herpesvirus 8, Human. Lymphoma, Primary Effusion / genetics. Lymphoma, Primary Effusion / virology

[MeSH-minor] Angiopoietin-1 / genetics. Cell Line, Tumor. Gene Expression Profiling. Humans

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[Copyright] Copyright 2010 Elsevier Inc. All rights reserved.

(PMID = 20175997.001).

[ISSN] 1090-2104

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Angiopoietin-1

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] PEL: an unbiased method for estimating age-dependent genetic disease risk from pedigree data unselected for family history.

Providing valid risk estimates of a genetic disease with variable age of onset is a major challenge for prevention strategies.

This article focuses on ascertainment through at least one affected and presents an estimation method based on maximum likelihood, called the Proband's phenotype exclusion likelihood or PEL for estimating age-dependent penetrance using disease status and genotypic information of family members in pedigrees unselected for family history.

We studied the properties of the PEL and compared with another method, the prospective likelihood, in terms of bias and efficiency in risk estimate.

For that purpose, family samples were simulated under various disease risk models and under various ascertainment patterns.

We showed that, whatever the genetic model and the ascertainment scheme, the PEL provided unbiased estimates, whereas the prospective likelihood exhibited some bias in a number of situations.

As an illustration, we estimated the disease risk for transthyretin amyloid neuropathy from a French sample and a Portuguese sample and for BRCA1/2 associated breast cancer from a sample ascertained on early-onset breast cancer cases.

[MeSH-minor] Age Factors. Amyloid Neuropathies / genetics. Bias (Epidemiology). Breast Neoplasms / genetics. France. Genes, BRCA1. Genes, BRCA2. Humans. Likelihood Functions. Models, Genetic. Models, Statistical. Pedigree. Phenotype. Portugal. Prealbumin / genetics. Risk

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[Copyright] 2008 Wiley-Liss, Inc.

[Cites] Genomics. 1999 Dec 15;62(3):369-76 [10644434.001]

[Cites] Eur J Hum Genet. 2007 Aug;15(8):831-6 [17473834.001]

[Cites] J Med Genet. 2001 Jan;38(1):43-7 [11332399.001]

[Cites] J Med Genet. 2002 May;39(5):335-9 [12011152.001]

[Cites] Genet Epidemiol. 2003 Apr;24(3):173-80 [12652521.001]

[Cites] J Med Genet. 2003 Nov;40(11):e120 [14627687.001]

[Cites] Genet Epidemiol. 2004 Sep;27(2):109-17 [15305327.001]

[Cites] Hum Hered. 1971;21(6):523-42 [5149961.001]

[Cites] Clin Genet. 1977 Oct;12(4):208-12 [334399.001]

[Cites] Genet Epidemiol. 1990;7(6):391-407 [2292365.001]

[Cites] Am J Hum Genet. 1995 Jan;56(1):265-71 [7825587.001]

[Cites] Am J Hum Genet. 1995 Jan;56(1):33-43 [7825595.001]

[Cites] Genet Epidemiol. 1995;12(1):13-25 [7713397.001]

[Cites] Hum Mol Genet. 1997 Jan;6(1):105-10 [9002677.001]

[Cites] Am J Hum Genet. 1997 May;60(5):1021-30 [9150149.001]

[Cites] Am J Hum Genet. 1998 Mar;62(3):676-89 [9497246.001]

[Cites] Am J Epidemiol. 1998 Oct 1;148(7):623-30 [9778168.001]

[Cites] Ann Oncol. 1998 Sep;9(9):939-50 [9818066.001]

[Cites] Genet Epidemiol. 1999;16(1):15-39 [9915565.001]

[Cites] Am J Hum Genet. 1959 Mar;11(1):1-16 [13626932.001]

[Cites] Genes Chromosomes Cancer. 2005 Aug;43(4):404-13 [15887246.001]

[Cites] Am J Hum Genet. 2000 Mar;66(3):1119-31 [10712222.001]

(PMID = 19089844.001).

[ISSN] 1098-2272

[Journal-full-title] Genetic epidemiology

[ISO-abbreviation] Genet. Epidemiol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Prealbumin

[Other-IDs] NLM/ HALMS358140; NLM/ PMC3108000

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cloning and preliminary characterization of a GATC-specific beta2-class DNA:m6A methyltransferase encoded by transposon Tn1549 from Enterococcus spp.

A recent study revealed a subfamily of N6-adenine (m6A) methyltransferases that comprises a few functionally studied eukaryotic members acting on mRNA and prokaryotic members acting on DNA as well as numerous uncharacterized open reading frames.

Here, we report cloning and functional characterization of a prokaryotic member of this family encoded by transposon Tn1549 from Enterococcus spp.

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(PMID = 16450842.001).

[ISSN] 1733-1331

[Journal-full-title] Polish journal of microbiology

[ISO-abbreviation] Pol. J. Microbiol.

[Language] ENG

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Poland

[Chemical-registry-number] 0 / DNA Transposable Elements; 0 / DNA, Bacterial; EC 2.1.1.72 / Site-Specific DNA-Methyltransferase (Adenine-Specific)

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pulmonary evaluation of permissible exposure limit of syntroleum S-8 synthetic jet fuel in mice.

No significant changes in respiratory permeability were exhibited, indicating that there was no loss of epithelial barrier integrity following S-8 exposure.

However, morphological examination and morphometric analysis of distal lung tissue, by using transmission electron microscopy, revealed cellular damage in alveolar type II epithelial cells, with significant increases in volume density of lamellar bodies/vacuoles at 352 and 616 S-8 mg/m(3).

Moreover, terminal bronchiolar Clara injury, as evidenced by apical membrane blebs, was observed at relatively low concentrations, suggesting if this synthetic jet fuel is utilized, the current permissible exposure limit of 350 mg/m(3) for hydrocarbon fuels should cautiously be applied.

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[Cites] Toxicol Pathol. 2000 Sep-Oct;28(5):656-63 [11026600.001]

[Cites] Electrophoresis. 1999 Dec;20(18):3659-69 [10612293.001]

[Cites] Toxicol Ind Health. 2001 Feb;17(1):23-9 [12004922.001]

[Cites] Toxicology. 2002 Jun 14;175(1-3):235-45 [12049851.001]

[Cites] Toxicol Sci. 2003 Dec;76(2):347-56 [14514957.001]

[Cites] Toxicology. 2004 Apr 15;197(2):139-47 [15003324.001]

[Cites] Toxicol Lett. 2004 Apr 1;149(1-3):301-8 [15093277.001]

[Cites] J Toxicol Environ Health A. 2004 Jul 23;67(14):1109-29 [15205027.001]

[Cites] Toxicol Appl Pharmacol. 1984 Aug;75(1):44-51 [6464021.001]

[Cites] Scand J Work Environ Health. 1985 Dec;11(6):433-7 [4095521.001]

[Cites] Am J Pathol. 1986 Jun;123(3):454-64 [3717299.001]

[Cites] Hepatology. 1995 May;21(5):1361-72 [7737643.001]

[Cites] J Appl Toxicol. 1996 May-Jun;16(3):197-200 [8818858.001]

[Cites] Toxicol Ind Health. 1997 Jan-Feb;13(1):43-55 [9098949.001]

[Cites] J Occup Environ Med. 1997 Jul;39(7):623-32 [9253723.001]

[Cites] Am J Physiol. 1999 Feb;276(2 Pt 1):L229-38 [9950884.001]

[Cites] Am J Respir Cell Mol Biol. 1999 Jul;21(1):44-53 [10385592.001]

[Cites] Toxicol Sci. 1999 Sep;51(1):119-25 [10496683.001]

[Cites] J Chromatogr A. 2005 Nov 4;1093(1-2):11-20 [16233866.001]

[Cites] Environ Health Perspect. 2006 Feb;114(2):182-5 [16451852.001]

[Cites] J Toxicol Sci. 2006 Aug;31(3):219-28 [16960432.001]

[Cites] Am J Respir Cell Mol Biol. 2006 Oct;35(4):479-87 [16690985.001]

[Cites] Int J Toxicol. 2007 Jul-Aug;26(4):325-9 [17661223.001]

[Cites] Toxicol Sci. 2007 Dec;100(2):415-22 [17890764.001]

[Cites] J Appl Toxicol. 2008 May;28(4):543-53 [17966119.001]

[Cites] Toxicology. 2008 Dec 5;254(1-2):106-11 [18930109.001]

[Cites] Am J Respir Cell Mol Biol. 1996 Jul;15(1):1-8 [8679213.001]

[Cites] Toxicol Sci. 2000 Dec;58(2):290-8 [11099641.001]

(PMID = 19357071.001).

[ISSN] 1096-0929

[Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology

[ISO-abbreviation] Toxicol. Sci.

[Language] ENG

[Grant] United States / NIEHS NIH HHS / ES / P30 ES006694; United States / NIEHS NIH HHS / ES / ES06694

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Hydrocarbons; 0 / S-8 fuel

[Other-IDs] NLM/ PMC2683924

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Subtype C1 persistent infection of HHV-8 in a PEL patient.

PEL, a rare type of lymphoma constituting less than 5% of NHLs, has been recently identified as a distinct clinical and pathological entity among the B-cell lymphomas, with characteristic morphologic, immunophenotypic, molecular and viral features.

Using a combination of clinical, morphological, immunohistochemical features and molecular biology techniques in this study we document a PEL case with persistent HHV-8 of genotype C1 infection.

[MeSH-minor] Adult. Amino Acid Sequence. Base Sequence. Follow-Up Studies. Genotype. Greece / ethnology. Hodgkin Disease. Humans. Male. Molecular Sequence Data. Phylogeny. Sequence Alignment. Viral Proteins / chemistry. Viral Proteins / genetics

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(PMID = 16194897.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / K1 protein, Human herpesvirus 8; 0 / Viral Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Detection and sequence analysis of an altered pectate lyase gene in Pseudomonas syringae pv. glycinea and related bacteria.

Pectate lyase (PL) is a potent cell wall-degrading enzyme known to play a role in the microbial infection of plants.

However, the PL gene (pel) was detected by Southern hybridization in four out of four P. syringae pv. glycinea strains examined.

A P. syringae pv. glycinea pel gene was cloned, sequenced, and predicted to encode a protein sharing 70%-90% identity in amino acid sequence with PLs produced by pectolytic pseudomonads and xanthomonads.

A series of amino acid and nucleotide sequence analyses reveal that (i) the predicted P. syringae pv. glycinea PL contains two regions in the amino acid sequence that may affect the formation of a beta-helix structure important for the enzyme activity, and (ii) the P. syringae pv. glycinea pel gene contains a single-base insertion, a double-base insertion, and an 18-bp deletion, which can lead to the synthesis of an inactive PL protein.

The altered pel sequence was also detected by polymerase chain reaction and nucleotide sequencing in the genomes of other pathovars of P. syringae, including phaseolicola and tagetis.

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(PMID = 17215896.001).

[ISSN] 0008-4166

[Journal-full-title] Canadian journal of microbiology

[ISO-abbreviation] Can. J. Microbiol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Canada

[Chemical-registry-number] EC 4.2.2.- / Polysaccharide-Lyases; EC 4.2.2.2 / pectate lyase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Integration of two essential virulence modulating signals at the Erwinia chrysanthemi pel gene promoters: a role for Fis in the growth-phase regulation.

Production of the essential virulence factors, called pectate lyases (Pels), in the phytopathogenic bacterium Erwinia chrysanthemi is controlled by a complex regulation system and responds to various stimuli, such as the presence of pectin or plant extracts, growth phase, temperature and iron concentration.

Eight regulators modulating the expression of the pel genes (encoding Pels) have been characterized.

Although many studies have been carried out, the mechanisms of control of Pel production by growth phase have not yet been elucidated.

Here we report that a fis mutant of E. chrysanthemi showed a strong increase in transcription of the pel genes during exponential growth whereas induction of expression in the parental strain occurred at the end of exponential growth.

This reveals that Fis acts to prevent an efficient transcription of pel genes at the beginning of exponential growth and also provides evidence of the involvement of Fis in the growth-phase regulation of the pel genes.

By using in vitro DNA-protein interactions and transcription experiments, we find that Fis directly represses the pel gene expression at the transcription initiation step.

In addition, we show that Fis acts in concert with KdgR, the main repressor responding to the presence of pectin compounds, to shut down the pel gene transcription.

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(PMID = 18028312.001).

[ISSN] 0950-382X

[Journal-full-title] Molecular microbiology

[ISO-abbreviation] Mol. Microbiol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Bacterial Proteins; 0 / KdgR protein, Erwinia chrysanthemi; 0 / Repressor Proteins; 0 / Transcription Factors; 9007-49-2 / DNA; EC 4.2.2.- / PelE protein, Erwinia chrysanthemi; EC 4.2.2.- / Polysaccharide-Lyases; EC 4.2.2.2 / pectate lyase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Antisense inhibition of a pectate lyase gene supports a role for pectin depolymerization in strawberry fruit softening.

It has been reported previously that inhibiting the expression of pectate lyase genes by antisense technology in strawberry (Fragaria x ananassa Duch.) fruit resulted in prolonged fruit firmness.

In this present study, three independent transgenic lines were identified exhibiting a greater than 90% reduction in pectate lyase transcript abundance.

These results indicate that pectate lyase plays an important degradative role in the primary wall and middle lamella in ripening strawberry fruit, and should be included in synergistic models of cell wall disassembly.

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[Cites] J Exp Bot. 2001 Aug;52(361):1635-45 [11479328.001]

[Cites] Plant Mol Biol. 2001 Sep;47(1-2):311-40 [11554479.001]

[Cites] Planta. 2001 Nov;214(1):11-21 [11762160.001]

[Cites] Planta. 2001 Dec;214(2):257-64 [11800390.001]

[Cites] Plant Physiol. 2002 Feb;128(2):751-9 [11842178.001]

[Cites] J Exp Bot. 2002 Oct;53(377):2115-9 [12324535.001]

[Cites] Plant Physiol. 2007 Aug;144(4):1693-6 [17687051.001]

[Cites] Planta. 2003 Oct;217(6):951-61 [12838420.001]

[Cites] Plant Physiol. 1997 Jul;114(3):1071-6 [9232883.001]

[Cites] Plant Mol Biol. 1997 Aug;34(6):867-77 [9290639.001]

[Cites] Anal Biochem. 1998 Mar 15;257(2):107-11 [9514779.001]

[Cites] Plant Physiol Biochem. 2004 Dec;42(10):823-31 [15596102.001]

[Cites] Plant Physiol. 2007 Jun;144(2):1012-28 [17449643.001]

[Cites] J Exp Bot. 2003 Feb;54(383):633-45 [12554706.001]

(PMID = 18522930.001).

[ISSN] 1460-2431

[Journal-full-title] Journal of experimental botany

[ISO-abbreviation] J. Exp. Bot.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Pectins; 0 / Plant Proteins; 9000-69-5 / pectin; EC 4.2.2.- / Polysaccharide-Lyases; EC 4.2.2.2 / pectate lyase

[Other-IDs] NLM/ PMC2486476

[Keywords] NOTNLM ; Cell wall / Fragaria / fruit ripening / pectate lyase / pectinases / strawberry

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Development of permissible exposure limits: the California experience.

The California OSHA Airborne Contaminant Advisory Committee reviewed several hundred substances and recommended occupational exposure limits with the intent of worker and employer protection.

[MeSH-major] Advisory Committees / organization & administration. Hazardous Substances / standards. Occupational Exposure / standards. Occupational Health / legislation & jurisprudence

[MeSH-minor] Animals. California. Communication. Humans. Maximum Allowable Concentration. National Institute for Occupational Safety and Health (U.S.) / standards. No-Observed-Adverse-Effect Level. Program Development. United States

MedlinePlus Health Information. consumer health - Occupational Health.

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(PMID = 16967831.001).

[ISSN] 1077-3525

[Journal-full-title] International journal of occupational and environmental health

[ISO-abbreviation] Int J Occup Environ Health

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Hazardous Substances

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Organ-specific, developmental, hormonal and stress regulation of expression of putative pectate lyase genes in Arabidopsis.

Pectate lyases catalyse the eliminative cleavage of de-esterified homogalacturonan in pectin, a major component of the primary cell walls in higher plants.

In the completed genome of Arabidopsis, there are 26 genes (AtPLLs) that encode pectate lyase-like proteins.

Interestingly, all PLL genes are expressed in flowers.

Analysis of expression of all PLL genes in seedlings treated with hormones, abiotic stresses and elicitors of defense responses revealed significant changes in the expression of some PLLs without affecting the other PLLs.

The stability of transcripts of PLLs varied considerably among different genes.

[MeSH-major] Arabidopsis / genetics. Arabidopsis Proteins / genetics. Gene Expression Regulation, Plant. Polysaccharide-Lyases / genetics

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(PMID = 17447910.001).

[ISSN] 0028-646X

[Journal-full-title] The New phytologist

[ISO-abbreviation] New Phytol.

[Language] eng

[Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] England

[Chemical-registry-number] 0 / Arabidopsis Proteins; 0 / Deoxyadenosines; 0 / RNA, Messenger; 73-03-0 / cordycepin; EC 4.2.2.- / Polysaccharide-Lyases; EC 4.2.2.2 / pectate lyase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Efficient secretory expression of an alkaline pectate lyase gene from Bacillus subtilis in E. coli and the purification and characterization of the protein.

The gene encoding pectate lyase (PL) from Bacillus subtilis WSHB04-02 was amplified by PCR, fused with a periplasmic secretion signal peptide sequence, pelB, from pET22b(+), cloned and expressed in Escherichia coli cells using a temperature control vector, pHsh.

[MeSH-minor] Enzyme Activation. Enzyme Stability. Gene Expression Regulation, Bacterial / physiology. Gene Expression Regulation, Enzymologic / physiology. Genetic Enhancement / methods. Recombinant Proteins / biosynthesis. Recombinant Proteins / chemistry

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(PMID = 17237974.001).

[ISSN] 1573-6776

[Journal-full-title] Biotechnology letters

[ISO-abbreviation] Biotechnol. Lett.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Recombinant Proteins; EC 4.2.2.- / Polysaccharide-Lyases; EC 4.2.2.2 / pectate lyase

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Sub classification and clinico-hematological correlation of 40 cases of acute erythroleukemia - can proerythroblast/myeloblast and proerythroblast/total erythroid cell ratios help subclassify?

The clinico-hematological profile of 40 cases of acute erythroleukemia (AEL) was evaluated.

These were subclassified into three types, namely AML M6a, M6b and M6c based on the myeloblast and proerythroblast percentages.

As AEL is biologically an "erythroid predominant" disease, two ratios (PE/MB, PE/TEC) with proerythroblasts as numerator have been formulated.

An attempt has been made to assess the difference in these ratios in subclassified AEL.

There were 29 M6a, 2M6b,and 9 M6 c patients, which were subclassified using the criteria proposed by Mazzella et al.

The incidence of AEL in our study was 3.7%, predominantly affecting males with a predilection to younger age in contrast to Western studies.

Both PE/MB and PE/TEC ratios were higher in M6b and M6c in comparison to M6a.

The subclassification of AEL becomes essential especially in the era of lineage-targeted therapies, which can lead to the development and use of erythroid specific treatments in the near future.

[MeSH-major] Leukemia, Erythroblastic, Acute / classification

[MeSH-minor] Adult. Age Factors. Aged. Cell Count. Erythroblasts. Erythroid Cells. Female. Granulocyte Precursor Cells. Humans. Incidence. Male. Middle Aged. Sex Factors

Genetic Alliance. consumer health - Acute Erythroleukemia.

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(PMID = 17852448.001).

[ISSN] 1607-8454

[Journal-full-title] Hematology (Amsterdam, Netherlands)

[ISO-abbreviation] Hematology

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] In vivo comparison of epithelial responses for S-8 versus JP-8 jet fuels below permissible exposure limit.

This study was designed to characterize and compare the pulmonary effects in distal lung from a low-level exposure to jet propellant-8 fuel (JP-8) and a new synthetic-8 fuel (S-8).

A pulmonary function test performed 24h after the final exposure indicated that there was a significant increase in expiratory lung resistance in the S-8 mice, whereas JP-8 mice had significant increases in both inspiratory and expiratory lung resistance compared to control values.

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[Cites] Electrophoresis. 1999 Dec;20(18):3659-69 [10612293.001]

[Cites] Toxicology. 2004 Apr 15;197(2):139-47 [15003324.001]

[Cites] Toxicol Sci. 2000 Dec;58(2):290-8 [11099641.001]

[Cites] Am J Physiol Lung Cell Mol Physiol. 2002 May;282(5):L1075-81 [11943673.001]

[Cites] Toxicol Ind Health. 2001 Feb;17(1):23-9 [12004922.001]

[Cites] Am J Respir Cell Mol Biol. 2002 Aug;27(2):170-8 [12151308.001]

[Cites] Toxicol Sci. 2003 Dec;76(2):347-56 [14514957.001]

[Cites] J Med Dent Sci. 2003 Sep;50(3):195-202 [15074357.001]

[Cites] Toxicol Lett. 2004 Apr 1;149(1-3):301-8 [15093277.001]

[Cites] J Toxicol Environ Health A. 2004 Jul 23;67(14):1109-29 [15205027.001]

[Cites] Acta Psychiatr Scand. 1979 Jul;60(1):39-49 [474176.001]

[Cites] Acta Psychiatr Scand Suppl. 1983;303:55-67 [6575584.001]

[Cites] Toxicol Appl Pharmacol. 1984 Aug;75(1):44-51 [6464021.001]

[Cites] Scand J Work Environ Health. 1985 Dec;11(6):433-7 [4095521.001]

[Cites] Am J Pathol. 1986 Jun;123(3):454-64 [3717299.001]

[Cites] Toxicol Ind Health. 1995 May-Jun;11(3):325-36 [7482572.001]

[Cites] Am J Respir Cell Mol Biol. 1996 Jul;15(1):1-8 [8679213.001]

[Cites] J Appl Toxicol. 1996 May-Jun;16(3):197-200 [8818858.001]

[Cites] Toxicol Ind Health. 1997 Jan-Feb;13(1):43-55 [9098949.001]

[Cites] J Occup Environ Med. 1997 Jul;39(7):623-32 [9253723.001]

[Cites] Am J Physiol. 1999 Feb;276(2 Pt 1):L229-38 [9950884.001]

[Cites] Drug Chem Toxicol. 1999 Feb;22(1):155-64 [10189576.001]

[Cites] Am J Respir Cell Mol Biol. 1999 Jul;21(1):44-53 [10385592.001]

[Cites] Toxicol Sci. 1999 Sep;51(1):119-25 [10496683.001]

[Cites] Phys Med Biol. 2005 Apr 7;50(7):1405-19 [15798332.001]

[Cites] J Chromatogr A. 2005 Nov 4;1093(1-2):11-20 [16233866.001]

[Cites] Environ Health Perspect. 2006 Feb;114(2):182-5 [16451852.001]

[Cites] J Toxicol Sci. 2006 Aug;31(3):219-28 [16960432.001]

[Cites] Am J Respir Cell Mol Biol. 2006 Oct;35(4):479-87 [16690985.001]

[Cites] Int J Toxicol. 2007 Jul-Aug;26(4):325-9 [17661223.001]

[Cites] J Appl Toxicol. 2008 May;28(4):543-53 [17966119.001]

[Cites] Toxicol Pathol. 2000 Sep-Oct;28(5):656-63 [11026600.001]

(PMID = 18930109.001).

[ISSN] 0300-483X

[Journal-full-title] Toxicology

[ISO-abbreviation] Toxicology

[Language] ENG

[Grant] United States / NIEHS NIH HHS / ES / ES006694-14; United States / NIEHS NIH HHS / ES / P30 ES006694; United States / NIEHS NIH HHS / ES / ES06694; United States / NIEHS NIH HHS / ES / P30 ES006694-14

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Ireland

[Chemical-registry-number] 0 / Hydrocarbons; 0 / JP8 aviation fuel; 0 / S-8 fuel

[Other-IDs] NLM/ NIHMS208577; NLM/ PMC2927360

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pure erythroid leukemia with hemophagocytosis.

Biochemistry showed increased ferritin levels.

Pure erythroid leukemia with hemophagocytic syndrome (HPS) was diagnosed.

Complete remission was attained, and HPS also improved.

However, leukemia relapsed during chemotherapy and the patient died.

This is the first report of pure erythroid leukemia complicated with HPS.

[MeSH-major] Leukemia, Erythroblastic, Acute / complications. Lymphohistiocytosis, Hemophagocytic / etiology

Hazardous Substances Data Bank. CYTARABINE .

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(PMID = 19755777.001).

[ISSN] 1349-7235

[Journal-full-title] Internal medicine (Tokyo, Japan)

[ISO-abbreviation] Intern. Med.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Antineoplastic Agents; 04079A1RDZ / Cytarabine; X4W7ZR7023 / Methylprednisolone; ZRP63D75JW / Idarubicin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Primary effusion lymphomas (PEL) form a subset of AIDS-related lymphomas and usually have a poor prognosis.

Although Kaposi's sarcoma-associated herpes virus (KSHV) is often associated with PEL, very little is known about the exact mechanisms or causative effects of these associations.

We investigated the chromosomal imbalances in six KSHV-positive PEL cell lines using comparative genomic hybridization analysis.

The recurrent nature of the gains found in these chromosomal regions suggests that these imbalances play roles in the pathogenesis of PEL.

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[Cites] Blood. 2003 Mar 1;101(5):1956-61 [12406869.001]

[Cites] J Infect Dis. 1999 Nov;180(5):1466-76 [10515805.001]

[Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):305-19 [16075461.001]

[Cites] J Clin Virol. 2000 May;16(3):215-24 [10738140.001]

[Cites] Arch Pathol Lab Med. 2000 Jun;124(6):824-6 [10835513.001]

[Cites] Recent Results Cancer Res. 2002;159:27-37 [11785841.001]

[Cites] Hematol J. 2001;2(3):172-9 [11920242.001]

[Cites] Leuk Lymphoma. 2002 Mar;43(3):595-601 [12002764.001]

[Cites] AIDS Patient Care STDS. 2004 Feb;18(2):67-73 [15006181.001]

[Cites] J Exp Med. 2004 Apr 5;199(7):993-1003 [15067035.001]

[Cites] Cancer Res. 2004 Jun 15;64(12):4064-8 [15205312.001]

[Cites] J Med Genet. 1999 Jul;36(7):511-7 [10424810.001]

(PMID = 17116491.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA096512; United States / NCI NIH HHS / CA / R01 CA096512-02; United States / NCI NIH HHS / CA / R01 CA096512-03; United States / NCI NIH HHS / CA / R01 CA124332; United States / NCI NIH HHS / CA / CA096512-01A2; United States / NCI NIH HHS / CA / CA096512-02; United States / NCI NIH HHS / CA / R01 CA124332-01A2; United States / NCI NIH HHS / CA / R01 CA096512-01A2; United States / NCI NIH HHS / CA / R01 CA096512-04; United States / NCI NIH HHS / CA / R01 CA132637

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Other-IDs] NLM/ NIHMS165930; NLM/ PMC2799290

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Primary effusion lymphoma (PEL) is an aggressive neoplasm caused by human herpes virus-8 infection, and is generally resistant to chemotherapy.

Hybrid liposomes, composed of dimyristoylphosphatidylcholine (DMPC) and polyoxyethylene (21) dodecyl ether (C12(EO)21) (HL-21), were rapidly accumulated in the membrane of PEL cells.

HL-21 also increased membrane fluidity of PEL cells, and induced caspase-3 activation along with cell death.

These results suggest that HL-21 should be an effective and attractive regent for PEL treatment.

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[Copyright] 2010 Elsevier Inc. All rights reserved.

(PMID = 20138834.001).

[ISSN] 1090-2104

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Liposomes; 0AWH8BFG9A / polidocanol; 30IQX730WE / Polyethylene Glycols; U86ZGC74V5 / Dimyristoylphosphatidylcholine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Gene alteration and precursor and mature microRNA transcription changes contribute to the miRNA signature of primary effusion lymphoma.

MicroRNAs are regulated by gene alteration, transcription, and processing.

Thus far, few studies have simultaneously assessed all 3 levels of regulation.

Using real-time quantitative polymerase chain reaction (QPCR)-based arrays, we determined changes in gene copy number, pre-miRNA, and mature miRNA levels for the largest set of primary effusion lymphomas (PELs) to date.

We detected PEL-specific miRNA gene amplifications, and concordant changes in pre-miRNA and mature miRNA.

We identified 68 PEL-specific miRNAs.

This defines the miRNA signature of PEL and shows that transcriptional regulation of pre-miRNA as well as mature miRNA levels contribute nonredundant information that can be used for the classification of human tumors.

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[Cites] Science. 2001 Aug 3;293(5531):834-8 [11452083.001]

[Cites] Nature. 2007 Dec 13;450(7172):1096-9 [18075594.001]

[Cites] Bioinformatics. 2002 Nov;18(11):1454-61 [12424116.001]

[Cites] Genes Dev. 2003 Feb 15;17(4):438-42 [12600936.001]

[Cites] Blood. 2003 May 15;101(10):4115-21 [12531789.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9779-84 [12902540.001]

[Cites] Nature. 2003 Sep 25;425(6956):415-9 [14508493.001]

[Cites] Science. 2004 Jan 2;303(5654):83-6 [14657504.001]

[Cites] Nucleic Acids Res. 2004;32(4):e43 [14985473.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):2999-3004 [14973191.001]

[Cites] Genes Dev. 2004 Mar 1;18(5):504-11 [15014042.001]

[Cites] J Clin Microbiol. 2004 Apr;42(4):1511-8 [15070997.001]

[Cites] Cancer Res. 2004 Jul 15;64(14):4790-9 [15256448.001]

[Cites] Mol Cell. 2004 Jul 23;15(2):185-97 [15260970.001]

[Cites] Nature. 2004 Sep 16;431(7006):343-9 [15372041.001]

[Cites] Methods Mol Biol. 2005;292:449-80 [15507725.001]

[Cites] N Engl J Med. 1995 May 4;332(18):1186-91 [7700311.001]

[Cites] Nat Med. 1997 Mar;3(3):293-8 [9055856.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Mar 8;102(10):3627-32 [15738415.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Apr 12;102(15):5570-5 [15800047.001]

[Cites] Nat Methods. 2005 Apr;2(4):269-76 [15782219.001]

[Cites] Nucleic Acids Res. 2005;33(8):2697-706 [15891114.001]

[Cites] Nature. 2005 Jun 9;435(7043):828-33 [15944707.001]

[Cites] J Virol. 2005 Jul;79(14):9301-5 [15994824.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13944-9 [16166262.001]

[Cites] Nucleic Acids Res. 2005;33(17):5394-403 [16192569.001]

[Cites] Nucleic Acids Res. 2005;33(21):e182 [16314296.001]

[Cites] J Virol. 2006 Jun;80(11):5321-6 [16699012.001]

[Cites] Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9136-41 [16754881.001]

[Cites] Blood. 2006 Nov 1;108(9):3068-71 [16849646.001]

[Cites] Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945.001]

[Cites] Cancer Genet Cytogenet. 2006 Dec;171(2):119-21 [17116491.001]

[Cites] Cancer Res. 2006 Dec 15;66(24):11590-3 [17178851.001]

[Cites] Int J Cancer. 2007 Mar 1;120(5):1046-54 [17149698.001]

[Cites] Nature. 2000 Mar 16;404(6775):293-6 [10749213.001]

[Cites] Arch Pathol Lab Med. 2000 Jun;124(6):824-6 [10835513.001]

[Cites] Cell. 2001 Jul 13;106(1):23-34 [11461699.001]

[Cites] J Infect Dis. 2007 Mar 1;195(5):645-59 [17262705.001]

[Cites] Oncogene. 2007 May 31;26(26):3769-76 [17173072.001]

[Cites] Cell. 2007 Jun 29;129(7):1401-14 [17604727.001]

[Cites] Oncogene. 2007 Jul 26;26(34):5017-22 [17297439.001]

[Cites] Nat Biotechnol. 2007 Sep;25(9):996-7 [17846629.001]

[Cites] J Virol. 2007 Dec;81(23):12836-45 [17881434.001]

[Cites] J Virol. 2002 Jun;76(12):6213-23 [12021355.001]

(PMID = 18079361.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA109232-05; United States / NCI NIH HHS / CA / R01 CA109232; United States / NIDCR NIH HHS / DE / DE018304; United States / NIDCR NIH HHS / DE / R01 DE018304-02; United States / NIDCR NIH HHS / DE / DE018304-01; United States / NIDCR NIH HHS / DE / R01 DE018304; United States / NCI NIH HHS / CA / R01 CA109232-05; United States / NIDCR NIH HHS / DE / R01 DE018304-01; United States / NCI NIH HHS / CA / CA109232; United States / NCI NIH HHS / CA / CA121947; United States / NIDCR NIH HHS / DE / R01 DE018304-03; United States / NIDCR NIH HHS / DE / DE018304-02; United States / NCI NIH HHS / CA / U01 CA121947; United States / NIDCR NIH HHS / DE / DE018304-03

[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 / MicroRNAs; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm

[Other-IDs] NLM/ PMC2234063

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Primary effusion lymphoma (PEL) is an incurable, aggressive B-cell malignancy that develops rapid resistance to conventional chemotherapy.

MG-132, a proteasome inhibitor, suppresses cell proliferation and induces apoptosis in several PEL cell lines.

Treatment of PEL cells with MG-132 results in downregulation of S-phase kinase protein 2 (SKP2) and accumulation of p27Kip1.

Furthermore, MG-132 treatment of PEL cells causes Bax conformational changes, leading to loss of mitochondrial membrane potential and release of cytochrome c to the cytosole.

Such cytochrome c release results in sequential activation of caspases and apoptosis, while pretreatment of PEL cells with universal inhibitor of caspases, z-VAD-fmk prevents cell death induced by MG-132.

Finally, our data demonstrated in PEL cells that MG-132 downregulates the expression of inhibitor of apoptosis proteins XIAP, cIAP1 and survivin.

Altogether, these findings suggest that MG-132 is a potent inducer of apoptosis of PEL cells via downregulation of SKP2 leading to accumulation of p27Kip1, resulting in cell cycle arrest and apoptosis and strongly suggest that targeting the proteasomal pathway may provide a novel therapeutic approach for the treatment of PEL.

[MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. Cyclin-Dependent Kinase Inhibitor p27 / metabolism. Gene Expression Regulation, Neoplastic. Leupeptins / pharmacology. Lymphoma, Primary Effusion / drug therapy. Lymphoma, Primary Effusion / pathology. S-Phase Kinase-Associated Proteins / metabolism

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(PMID = 19557642.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Antineoplastic Agents; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Leupeptins; 0 / Microtubule-Associated Proteins; 0 / S-Phase Kinase-Associated Proteins; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 9007-43-6 / Cytochromes c

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Primary effusion lymphoma (PEL) is a rare subtype of non-Hodgkin's lymphoma, which is associated with infection by Kaposi's sarcoma herpesvirus (KSHV)/human herpesvirus-8.

However, no structural abnormalities were found in the c-myc oncogene in PEL.

Given that c-Myc is often involved in lymphomagenesis, we hypothesized that it is deregulated in PEL.

We report that PEL cells have abnormally stable c-Myc protein.

Our data show that the impaired c-Myc degradation in PEL cells is associated with a significant underphosphorylation of c-Myc T58.

Conversely, when LANA is eliminated from PEL cells using RNA interference, GSK-3beta-mediated c-Myc T58 phosphorylation is restored.

The presence of c-Myc and LANA in GSK-3beta-containing complexes in PEL cells further confirms the significance of these interactions in naturally KSHV-infected cells.

[MeSH-minor] B-Lymphocytes / metabolism. B-Lymphocytes / virology. Cell Line. Glycogen Synthase Kinase 3 / metabolism. Humans. RNA Interference. Threonine / metabolism

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(PMID = 17310999.001).

[ISSN] 0950-9232

[Journal-full-title] Oncogene

[ISO-abbreviation] Oncogene

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA068939

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, Viral; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / latency-associated nuclear antigen; 2ZD004190S / Threonine; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Recent studies of acute erythroleukemias have reaffirmed DiGuglielmo's syndrome (M6a, myeloblast-predominant) and disease (M6b, pronormoblast-predominant).

A 20-year retrospective study was performed to identify cases demonstrating >or=50% erythrocytic component and <30% calculated blasts (FAB exclusion criteria) without underlying cause (96 cases).

[MeSH-major] Erythroblasts. Leukemia, Erythroblastic, Acute / pathology. Models, Statistical. Myelodysplastic Syndromes / pathology

[MeSH-minor] Age Factors. Disease-Free Survival. Erythrocyte Count. Erythrocytes / pathology. Granulocyte Precursor Cells / pathology. Humans. Male. Middle Aged. Multivariate Analysis. Platelet Count. Predictive Value of Tests. Prognosis. Retrospective Studies

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(PMID = 16755568.001).

[ISSN] 0361-8609

[Journal-full-title] American journal of hematology

[ISO-abbreviation] Am. J. Hematol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Pelargonidin (PEL), a common anthocyanidin with estrogenic activity, was tested in HL-60 cells for its genotoxicity and possible antigenotoxic effects against 4-nitroquinoline 1-oxide (NQO), a potent mutagen and carcinogen which induces oxidative stress.

To take into account potential interactions between phytochemicals within normal human nutrition, we evaluated a combination of PEL with the nonestrogenic phytochemical chlorogenic acid (CLA), one of the most abundant polyphenols in the human diet.

PEL (< or = 2 microM) and CLA (< or = 800 microM) were nongenotoxic in the micronucleus test.

We observed significant antigenotoxic effects against NQO with both compounds, but no additive interaction of PEL and CLA.

Flow cytometric analysis of oxidative stress revealed significant protection against NQO-induced oxidative stress by PEL, CLA, and their combination.

Furthermore, PEL and CLA prevented the NQO-induced reduction in GSH level.

In conclusion, the phytoestrogen PEL revealed antioxidative and antigenotoxic properties in HL-60 cells, but no significant additive interaction with the abundant nutritional polyphenol CLA under the tested conditions.

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(PMID = 17579891.001).

[ISSN] 1613-4125

[Journal-full-title] Molecular nutrition & food research

[ISO-abbreviation] Mol Nutr Food Res

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Anthocyanins; 0 / Antimutagenic Agents; 0 / Mutagens; 0 / Phytoestrogens; 318ADP12RI / Chlorogenic Acid; 56-57-5 / 4-Nitroquinoline-1-oxide; 7690-51-9 / pelargonidin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Diffuse large B-cell lymphoma initially manifested by massive ascites and a small gastric lesion, clinically mimicking primary effusion lymphoma (PEL) in the abdominal cavity: a case report and review of the literature on Japanese PEL patients].

The patient was treated with chemotherapy including rituximab (R-CHOP-ESHAP) and injection of methotrexate and dexamethasone into the medullary cavity as well as radiation to the whole brain, and achieved complete remission 4 months later.

[MeSH-major] Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Primary Effusion / diagnosis

[MeSH-minor] Ascites / complications. Diagnosis, Differential. Humans. Male. Middle Aged. Stomach Neoplasms / pathology

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(PMID = 18057856.001).

[ISSN] 0446-6586

[Journal-full-title] Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology

[ISO-abbreviation] Nihon Shokakibyo Gakkai Zasshi

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article; Review

[Publication-country] Japan

[Number-of-references] 40

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Primary effusion lymphoma (PEL) is a fatal malignancy, which typically presents as a lymphomatous effusion that later disseminates.

Rapamycin (Rapa), which targets mTOR (mammalian target of Rapa), is currently evaluated as a treatment for PEL, but the recent development of PEL in Rapa-treated post-transplant recipients questions the drug's use in PEL.

Here, we used a murine model of PEL effusion that mimics the human disease to investigate the anti-PEL activity of Rapa.

Initially, Rapa reduced PEL load compared with control mice, but most mice rapidly showed PEL progression.

Levels of VEGF, which promotes vascular permeability contributing to effusion formation, were significantly reduced in ascites of Rapa-treated mice compared with controls.

Expression of IL-10, the principal autocrine growth factor for PEL, was initially reduced in PEL from Rapa-treated mice but rapidly increased despite treatment.

We found that the hypoxic environment of ascites and Rapa cooperate in stimulating IL-10 expression in PEL, which likely contributes to the emergence of drug resistance.

These results identify Rapa an effective drug to reduce PEL effusions but illustrate the rapid development of drug resistance, which likely limits the efficacy of Rapa in PEL.

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[Cites] Blood. 1999 Dec 15;94(12):4247-54 [10590069.001]

[Cites] Am J Transplant. 2008 Mar;8(3):707-10 [18261181.001]

[Cites] Eur J Immunol. 2001 Feb;31(2):350-9 [11180098.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Feb 27;98(5):2604-9 [11226286.001]

[Cites] Blood. 2001 Nov 15;98(10):3042-9 [11698289.001]

[Cites] Nat Med. 2002 Feb;8(2):128-35 [11821896.001]

[Cites] Curr Opin Investig Drugs. 2002 Feb;3(2):295-304 [12020063.001]

[Cites] Cancer Res. 2003 Aug 1;63(15):4472-80 [12907620.001]

[Cites] J Clin Oncol. 2003 Nov 1;21(21):3948-54 [14581418.001]

[Cites] J Lab Clin Med. 1971 Dec;78(6):1006 [5131833.001]

[Cites] South Med J. 1981 May;74(5):585-9 [6787716.001]

[Cites] Cancer Res. 1995 Jan 15;55(2):376-85 [7529135.001]

[Cites] N Engl J Med. 1995 May 4;332(18):1186-91 [7700311.001]

[Cites] Blood. 1996 Jul 15;88(2):645-56 [8695812.001]

[Cites] Cancer Res. 1998 Jun 15;58(12):2652-60 [9635593.001]

[Cites] N Engl J Med. 1998 Aug 13;339(7):444-9 [9700178.001]

[Cites] Am J Pathol. 1998 Oct;153(4):1249-56 [9777956.001]

[Cites] J Biol Chem. 1998 Nov 13;273(46):30336-43 [9804796.001]

[Cites] Blood. 1999 Jun 15;93(12):4034-43 [10361100.001]

[Cites] Blood. 1999 Oct 15;94(8):2871-9 [10515891.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):904-8 [15640348.001]

[Cites] N Engl J Med. 2005 Mar 31;352(13):1317-23 [15800227.001]

[Cites] Curr Opin Cell Biol. 2005 Dec;17(6):596-603 [16226444.001]

[Cites] Cell. 2006 Feb 10;124(3):471-84 [16469695.001]

[Cites] J Physiol. 2006 Jul 1;574(Pt 1):275-81 [16675496.001]

[Cites] Cancer Cell. 2006 Aug;10(2):159-70 [16904613.001]

[Cites] Blood. 2007 Mar 1;109(5):2165-73 [17082322.001]

[Cites] Cancer Res. 2007 Mar 15;67(6):2408-13 [17363557.001]

[Cites] Transplantation. 2007 Apr 27;83(8):1114-21 [17452903.001]

[Cites] Cancer Cell. 2007 Jul;12(1):9-22 [17613433.001]

[Cites] Mol Cell. 1999 Dec;4(6):915-24 [10635317.001]

(PMID = 19554030.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] ENG

[Grant] United States / Intramural NIH HHS / / NIH0012215497; United States / PHS HHS / / NIH0012215497; United States / Intramural NIH HHS / /

[Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Interleukin-6; 0 / Vascular Endothelial Growth Factors; 130068-27-8 / Interleukin-10; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; W36ZG6FT64 / Sirolimus

[Other-IDs] NLM/ NIHMS113595; NLM/ PMC2940422

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

OBJECTIVE: To evaluate morphologic changes of the stratum internum of hooves from near-term fetal, newborn, and yearling horses.

PROCEDURES: Primary epidermal laminae (PEL) of the stratum internum were examined for evidence of architectural changes.

RESULTS: In near-term fetuses, the PEL had a homogeneous appearance and symmetric distribution around the hoof wall with no significant differences in PEL density between the toe and quarters.

However after birth, branched laminae at the toe formed within the first few weeks, which significantly increased PEL density at the toe, compared with the quarters.

In yearlings, morphology of the PEL differed from that in younger foals and the PEL density was significantly greater at the toe than the quarters.

The PEL density at the toe and medial and lateral quarters was significantly different from each other, as these PEL densities appeared to have been associated with conformation.

No significant differences in PEL densities between forefeet and hind feet were detected in any group.

CONCLUSIONS AND CLINICAL RELEVANCE: Findings indicate that the stratum internum of the inner hoof wall undergoes several morphologic changes shortly after birth.

The PEL become branched with a greater PEL density at the toe than the quarters.

In an asymmetric foot, more PEL were associated with the sloping side than the steep side of the foot.

Findings suggested that PEL growth may also occur by bifurcation as well as by mitosis from the coronet and that wall stress may be associated with increased PEL density.

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(PMID = 17144792.001).

[ISSN] 0002-9645

[Journal-full-title] American journal of veterinary research

[ISO-abbreviation] Am. J. Vet. Res.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of primary effusion lymphoma (PEL) and of Kaposi's sarcoma.

PEL is an aggressive proliferation of B cells with poor prognosis.

We evaluated both in vitro and in vivo the potential role of angiogenic factors secreted by PEL cells, that is, their interaction with endothelial cells and their implication in the invasive behavior of tumoral cells.

In vitro, PEL-induced angiogenesis is dependent on vascular endothelial growth factor (VEGF) and VEGF receptors.

However, although PEL cells produce VEGF and basic fibroblast growth factor (b-FGF) transcripts, they only secrete VEGF in vitro.

In vivo, very high levels of both VEGF and b-FGF were found in the ascitic fluid of NOD/SCID mice injected with PEL cells.

We then show evidence of cell adhesion and gap junction-mediated heterocellular communication between PEL cells and endothelial cells.

Finally, we show that PEL cells extravasate through the endothelial barrier and that the specific tyrosine kinase inhibitor of VEGF receptors, PTK-787/ZK-222584, the anti-VEGF antibody, bevacizumab or the gap junction inhibitor 18-alpha-glycyrrhetinic acid, partially attenuate PEL cell extravasation.

Angiogenesis, cell adhesion and communication likely contribute to the development of PEL and represent potential therapeutic targets.

[MeSH-minor] Animals. Cell Transformation, Viral. Coculture Techniques. Disease Models, Animal. Endothelial Cells / pathology. Gap Junctions / pathology. Humans. Mice. Neoplasms, Experimental. Paracrine Communication. Transplantation, Heterologous. Tumor Cells, Cultured

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(PMID = 18094712.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 103107-01-3 / Fibroblast Growth Factor 2