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1. Mameza MG, Lockard JM, Zamora E, Hillefors M, Lavina ZS, Kaplan BB: Characterization of the adaptor protein ARH expression in the brain and ARH molecular interactions. J Neurochem; 2007 Nov;103(3):927-41
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  • A yeast two hybrid screen for ARH protein interactions in mouse brain identified the following binders: amyloid precursor-like protein 1, low density lipoprotein receptor-related protein (LRP) 1, LRP8, and GABA receptor-associated protein-like 1.
  • [MeSH-minor] Animals. Axons / metabolism. Axons / ultrastructure. Cell Line. Cytoskeletal Proteins / metabolism. Decapodiformes / genetics. Decapodiformes / metabolism. Evolution, Molecular. Ganglia, Sympathetic / metabolism. Ganglia, Sympathetic / ultrastructure. Humans. Membrane Proteins / metabolism. Mice. Molecular Sequence Data. Protein Binding / physiology. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Receptors, LDL / metabolism. Sequence Homology, Amino Acid. Tumor Suppressor Proteins / metabolism


2. Hebda JA, Saraogi I, Magzoub M, Hamilton AD, Miranker AD: A peptidomimetic approach to targeting pre-amyloidogenic states in type II diabetes. Chem Biol; 2009 Sep 25;16(9):943-50
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  • For many systems, including islet amyloid polypeptide (IAPP) from type II diabetes, fibrillogenesis can be catalyzed by lipid bilayers.
  • Paradoxically, amyloid fibers are beta sheet rich while membrane-stabilized states are alpha-helical.
  • IS5 therefore represents a new approach to amyloid inhibition as the target is an assembly intermediate that may additionally restore functional IAPP expression.

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  • (PMID = 19778722.001).
  • [ISSN] 1879-1301
  • [Journal-full-title] Chemistry & biology
  • [ISO-abbreviation] Chem. Biol.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / F31 AG031612; United States / NIA NIH HHS / AG / AG031612; United States / NIGMS NIH HHS / GM / R01 GM069850; United States / NIDDK NIH HHS / DK / R21 DK079829; United States / NIGMS NIH HHS / GM / GM69850
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acetates; 0 / Aminopyridines; 0 / Amyloid; 0 / Insulin; 0 / Islet Amyloid Polypeptide; 0 / Lipid Bilayers
  • [Other-IDs] NLM/ NIHMS373226; NLM/ PMC3341621
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3. Fluhrer R, Grammer G, Israel L, Condron MM, Haffner C, Friedmann E, Böhland C, Imhof A, Martoglio B, Teplow DB, Haass C: A gamma-secretase-like intramembrane cleavage of TNFalpha by the GxGD aspartyl protease SPPL2b. Nat Cell Biol; 2006 Aug;8(8):894-6
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  • We demonstrate that SPPL2b utilizes multiple intramembrane cleavages to liberate the intracellular domain of tumor necrosis factor alpha (TNFalpha) into the cytosol and the carboxy-terminal counterpart into the extracellular space.
  • [MeSH-major] Aspartic Acid Endopeptidases / metabolism. Endopeptidases / metabolism. Intracellular Membranes / metabolism. Tumor Necrosis Factor-alpha / metabolism. Zebrafish Proteins / metabolism
  • [MeSH-minor] Amino Acid Sequence. Amyloid Precursor Protein Secretases. Binding Sites / genetics. Cell Line. Cytosol / chemistry. Cytosol / enzymology. Cytosol / metabolism. Humans. Molecular Sequence Data. Mutation / genetics. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization


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4. Nakamura T, Higashi S, Tomoda K, Tsukano M, Baba S: Efficacy of etanercept in patients with AA amyloidosis secondary to rheumatoid arthritis. Clin Exp Rheumatol; 2007 Jul-Aug;25(4):518-22
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  • OBJECTIVE: The efficacy of biological therapies in rheumatoid arthritis (RA) is well known, but their hypothetical benefit in amyloid A (AA) amyloidosis secondary to RA still remains to be considered.
  • We evaluated the efficacy and safety of etanercept in serum amyloid A (SAA) 1.3 allele Japanese patients with AA amyloidosis secondary to RA.
  • [MeSH-major] Amyloidosis / drug therapy. Amyloidosis / etiology. Arthritis, Rheumatoid / complications. Immunoglobulin G / therapeutic use. Immunosuppressive Agents / therapeutic use. Receptors, Tumor Necrosis Factor / therapeutic use


5. Atkins CM, Oliva AA Jr, Alonso OF, Pearse DD, Bramlett HM, Dietrich WD: Modulation of the cAMP signaling pathway after traumatic brain injury. Exp Neurol; 2007 Nov;208(1):145-58
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  • Traumatic axonal injury, characterized by beta-amyloid precursor protein deposits in the external capsule, was also significantly reduced in rolipram-treated animals.
  • Furthermore, levels of the pro-inflammatory cytokines, interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), were significantly decreased with rolipram treatment.

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  • (PMID = 17916353.001).
  • [ISSN] 0014-4886
  • [Journal-full-title] Experimental neurology
  • [ISO-abbreviation] Exp. Neurol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS042133-05; United States / NINDS NIH HHS / NS / NS042133-05; United States / NINDS NIH HHS / NS / NS42133; United States / NINDS NIH HHS / NS / NS30291; United States / NINDS NIH HHS / NS / NS056072-01A1; United States / NINDS NIH HHS / NS / R01 NS042133; United States / NINDS NIH HHS / NS / P50 NS030291-15; United States / NINDS NIH HHS / NS / R01 NS056072; United States / NINDS NIH HHS / NS / NS030291-15; United States / NINDS NIH HHS / NS / P50 NS030291; United States / NINDS NIH HHS / NS / R01 NS056072-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Interleukin-1beta; 0 / Phosphodiesterase 4 Inhibitors; 0 / Phosphodiesterase Inhibitors; 0 / Tumor Necrosis Factor-alpha; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; K676NL63N7 / Rolipram
  • [Other-IDs] NLM/ NIHMS34649; NLM/ PMC2141537
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6. Velez-Pardo C, Del Rio MJ: Avoidance of Abeta[(25-35)] / (H(2)O(2)) -induced apoptosis in lymphocytes by the cannabinoid agonists CP55,940 and JWH-015 via receptor-independent and PI3K-dependent mechanisms: role of NF-kappaB and p53. Med Chem; 2006 Sep;2(5):471-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Amyloid beta-Peptides / pharmacology. Apoptosis / drug effects. Cannabinoids / agonists. Hydrogen Peroxide / pharmacology. Lymphocytes / drug effects. NF-kappa B / metabolism. Peptide Fragments / pharmacology. Phosphatidylinositol 3-Kinases / metabolism. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 17017986.001).
  • [ISSN] 1573-4064
  • [Journal-full-title] Medicinal chemistry (Shāriqah (United Arab Emirates))
  • [ISO-abbreviation] Med Chem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Cannabinoids; 0 / Cyclohexanes; 0 / Cyclohexanols; 0 / Indoles; 0 / JHW 015; 0 / NF-kappa B; 0 / Peptide Fragments; 0 / Phenols; 0 / Protein Kinase Inhibitors; 0 / Receptors, Cannabinoid; 0 / Tumor Suppressor Protein p53; 0 / amyloid beta-protein (25-35); 83003-12-7 / 3-(2-hydroxy-4-(1,1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol; BBX060AN9V / Hydrogen Peroxide; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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7. Hinkle CL, Diestel S, Lieberman J, Maness PF: Metalloprotease-induced ectodomain shedding of neural cell adhesion molecule (NCAM). J Neurobiol; 2006 Oct;66(12):1378-95
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  • [MeSH-minor] Amyloid Precursor Protein Secretases / metabolism. Animals. Antigens, CD / metabolism. Cell Line, Tumor. Cerebral Cortex / cytology. Cerebral Cortex / embryology. Cerebral Cortex / metabolism. Disease Models, Animal. Down-Regulation / physiology. Enzyme Inhibitors / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Fibroblasts / cytology. Fibroblasts / metabolism. Membrane Proteins / metabolism. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neurites / metabolism. Neurites / ultrastructure. Protein Structure, Tertiary / physiology. Protein Tyrosine Phosphatases / antagonists & inhibitors. Protein Tyrosine Phosphatases / metabolism. Schizophrenia / genetics. Schizophrenia / metabolism. Schizophrenia / physiopathology

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  • [Copyright] (c) 2006 Wiley Periodicals, Inc.
  • (PMID = 16967505.001).
  • [ISSN] 0022-3034
  • [Journal-full-title] Journal of neurobiology
  • [ISO-abbreviation] J. Neurobiol.
  • [Language] eng
  • [Grant] United States / NIMH NIH HHS / MH / MH064065; United States / NINDS NIH HHS / NS / NS26620
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Enzyme Inhibitors; 0 / Membrane Proteins; 0 / Neural Cell Adhesion Molecules; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / Adam8 protein, mouse; EC 3.4.24.81 / Adam10 protein, mouse
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8. Yang X, Sheng W, He Y, Cui J, Haidekker MA, Sun GY, Lee JC: Secretory phospholipase A2 type III enhances alpha-secretase-dependent amyloid precursor protein processing through alterations in membrane fluidity. J Lipid Res; 2010 May;51(5):957-66
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  • [Title] Secretory phospholipase A2 type III enhances alpha-secretase-dependent amyloid precursor protein processing through alterations in membrane fluidity.
  • In the non-amyloidogenic pathway, amyloid precursor protein (APP) is cleaved by alpha-secretases to produce alpha-secretase-cleaved soluble APP (sAPP(alpha)) with neuroprotective and neurotrophic properties; therefore, enhancing the non-amyloidogenic pathway has been suggested as a potential pharmacological approach for the treatment of Alzheimer's disease.

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  • (PMID = 19805624.001).
  • [ISSN] 1539-7262
  • [Journal-full-title] Journal of lipid research
  • [ISO-abbreviation] J. Lipid Res.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / P01 AG018357; United States / NINDS NIH HHS / NS / R21 NS052385; United States / NIA NIH HHS / AG / 1P01 AG18357; United States / NINDS NIH HHS / NS / 1R21 NS052385
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Lysophosphatidylcholines; 27YG812J1I / Arachidonic Acid; 2V16EO95H1 / Palmitic Acid; EC 3.1.1.4 / Group III Phospholipases A2; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / Bace protein, rat
  • [Other-IDs] NLM/ PMC2853463
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9. Chen CH, Wang PH, Liu BH, Hsu HH, Mersmann HJ, Ding ST: Serum amyloid A protein regulates the expression of porcine genes related to lipid metabolism. J Nutr; 2008 Apr;138(4):674-9
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  • [Title] Serum amyloid A protein regulates the expression of porcine genes related to lipid metabolism.
  • Serum amyloid A protein (SAA) is an apolipoprotein that can replace apolipoprotein A1 (apoA1) as the major apolipoprotein of HDL.
  • SAA treatment also increased inflammatory cytokine gene expression (IL-6 and tumor necrosis factor alpha) and glycerol release (P < 0.05), indicating increased lipolysis.
  • [MeSH-major] Gene Expression Regulation / drug effects. Lipid Metabolism / drug effects. Lipid Metabolism / genetics. Serum Amyloid A Protein / pharmacology. Swine / genetics. Swine / metabolism

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  • (PMID = 18356319.001).
  • [ISSN] 1541-6100
  • [Journal-full-title] The Journal of nutrition
  • [ISO-abbreviation] J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Serum Amyloid A Protein; 25167-62-8 / Docosahexaenoic Acids
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11. Sun X, Wu WH, Liu Q, Chen MS, Yu YP, Ma Y, Zhao YF, Li YM: Hybrid peptides attenuate cytotoxicity of beta-amyloid by inhibiting its oligomerization: implication from solvent effects. Peptides; 2009 Jul;30(7):1282-7
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  • [Title] Hybrid peptides attenuate cytotoxicity of beta-amyloid by inhibiting its oligomerization: implication from solvent effects.
  • Abnormal assembly of monomeric beta-amyloid (Abeta) in Alzheimer's disease leads to the formation of most neurotoxic oligomers in vivo.
  • [MeSH-major] Amyloid beta-Peptides / chemistry. Amyloid beta-Peptides / toxicity. Neurons / drug effects. Peptides / chemistry. Peptides / pharmacology. Protein Multimerization / drug effects
  • [MeSH-minor] Amino Acid Motifs. Amino Acid Sequence. Animals. Cell Line, Tumor. Mice. Microscopy, Electron, Transmission. Molecular Sequence Data

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  • (PMID = 19397942.001).
  • [ISSN] 1873-5169
  • [Journal-full-title] Peptides
  • [ISO-abbreviation] Peptides
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Peptides
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12. Bräuner EV, Forchhammer L, Møller P, Barregard L, Gunnarsen L, Afshari A, Wåhlin P, Glasius M, Dragsted LO, Basu S, Raaschou-Nielsen O, Loft S: Indoor particles affect vascular function in the aged: an air filtration-based intervention study. Am J Respir Crit Care Med; 2008 Feb 15;177(4):419-25
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  • Secondary endpoints included hemoglobin, red blood cells, platelet count, coagulation factors, P-selectin, plasma amyloid A, C-reactive protein, fibrinogen, IL-6, tumor necrosis factor-alpha, protein oxidation measured as 2-aminoadipic semialdehyde in plasma, urinary 8-iso-prostaglandin F(2alpha), and blood pressure.


13. Wang CY, Wang T, Zheng W, Zhao BL, Danscher G, Chen YH, Wang ZY: Zinc overload enhances APP cleavage and Aβ deposition in the Alzheimer mouse brain. PLoS One; 2010;5(12):e15349
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  • BACKGROUND: Abnormal zinc homeostasis is involved in β-amyloid (Aβ) plaque formation and, therefore, the zinc load is a contributing factor in Alzheimer's disease (AD).
  • However, the involvement of zinc in amyloid precursor protein (APP) processing and Aβ deposition has not been well established in AD animal models in vivo.
  • [MeSH-major] Amyloid beta-Protein Precursor / metabolism. Zinc / metabolism
  • [MeSH-minor] Alzheimer Disease / metabolism. Animals. Cell Line, Tumor. Homeostasis. Humans. Learning. Male. Maze Learning. Memory. Mice. Mice, Transgenic. Models, Biological. Presenilin-1 / genetics. Risk Factors

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  • (PMID = 21179415.001).
  • [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 / Amyloid beta-Protein Precursor; 0 / Presenilin-1; J41CSQ7QDS / Zinc
  • [Other-IDs] NLM/ PMC3003690
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14. Gutwein P, Schramme A, Sinke N, Abdel-Bakky MS, Voss B, Obermüller N, Doberstein K, Koziolek M, Fritzsche F, Johannsen M, Jung K, Schaider H, Altevogt P, Ludwig A, Pfeilschifter J, Kristiansen G: Tumoural CXCL16 expression is a novel prognostic marker of longer survival times in renal cell cancer patients. Eur J Cancer; 2009 Feb;45(3):478-89
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  • Our immunohistochemical analysis on tissue microarray of renal cancer samples of 104 patients revealed that ADAM10 correlated significantly with tumour stage, pathological nodal status, M status and lymphangiosis carcinomatosa.
  • Importantly, high levels of CXCL16 expression in renal cancer tissue correlated with better survival of patients, and CXCL16 correlated inversely to the tumour stage.
  • [MeSH-major] ADAM Proteins / metabolism. Amyloid Precursor Protein Secretases / metabolism. Carcinoma, Renal Cell / metabolism. Chemokines, CXC / metabolism. Kidney Neoplasms / metabolism. Membrane Proteins / metabolism. Neoplasm Proteins / metabolism. Receptors, Chemokine / metabolism. Receptors, Scavenger / metabolism. Receptors, Virus / metabolism
  • [MeSH-minor] Adult. Biomarkers, Tumor / genetics. Cell Line, Tumor. Female. Gene Expression Regulation, Neoplastic / genetics. Humans. Immunohistochemistry. Male

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  • (PMID = 19070478.001).
  • [ISSN] 1879-0852
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CXCL16 protein, human; 0 / CXCR6 protein, human; 0 / Chemokines, CXC; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Receptors, Chemokine; 0 / Receptors, Scavenger; 0 / Receptors, Virus; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.81 / ADAM10 protein, human
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15. Greco SJ, Sarkar S, Johnston JM, Zhu X, Su B, Casadesus G, Ashford JW, Smith MA, Tezapsidis N: Leptin reduces Alzheimer's disease-related tau phosphorylation in neuronal cells. Biochem Biophys Res Commun; 2008 Nov 21;376(3):536-41
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  • Recently, it was shown that leptin can reduce amyloid beta levels both in vitro and in vivo.
  • Thus, leptin, which ameliorates both amyloid beta and tau-related pathological pathways, holds promise as a novel therapeutic for Alzheimer's disease.
  • [MeSH-minor] AMP-Activated Protein Kinases. Aminoimidazole Carboxamide / analogs & derivatives. Aminoimidazole Carboxamide / pharmacology. Cell Line, Tumor. Humans. Insulin / pharmacology. Multienzyme Complexes / antagonists & inhibitors. Multienzyme Complexes / metabolism. Phosphorylation / drug effects. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases / metabolism. Pyrazoles / pharmacology. Pyrimidines / pharmacology. Ribonucleotides / pharmacology. Signal Transduction

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  • (PMID = 18801339.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R43 AG029670; United States / NIA NIH HHS / AG / R43 AG029670-01A1; United States / NIA NIH HHS / AG / 1R43AG029670
  • [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 / (6-(4-(2-piperidin-1-ylethoxy)phenyl))-3-pyridin-4-ylpyrazolo(1,5-a)pyrimidine; 0 / Insulin; 0 / Leptin; 0 / Multienzyme Complexes; 0 / Pyrazoles; 0 / Pyrimidines; 0 / Ribonucleotides; 0 / tau Proteins; 360-97-4 / Aminoimidazole Carboxamide; EC 2.7.11.1 / AMP-Activated Protein Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; F0X88YW0YK / AICA ribonucleotide
  • [Other-IDs] NLM/ NIHMS74881; NLM/ PMC2577167
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16. Buchhave P, Zetterberg H, Blennow K, Minthon L, Janciauskiene S, Hansson O: Soluble TNF receptors are associated with Aβ metabolism and conversion to dementia in subjects with mild cognitive impairment. Neurobiol Aging; 2010 Nov;31(11):1877-84
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  • OBJECTIVE: There is evidence supporting that tumor necrosis factor receptor (TNFR)-signaling can induce production of beta-amyloid (Aβ) in the brain.
  • Moreover, amyloid-induced toxicity has been shown to be dependent on TNFR-signaling.
  • CONCLUSION: TNFR-signaling might be involved in the early pathogenesis of AD and VaD, and could be associated with beta-amyloid metabolism.
  • [MeSH-major] Alzheimer Disease / metabolism. Amyloid beta-Peptides / metabolism. Cognition Disorders / metabolism. Dementia, Vascular / metabolism. Receptors, Tumor Necrosis Factor, Type I / metabolism. Receptors, Tumor Necrosis Factor, Type II / metabolism

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  • [Copyright] Copyright © 2008 Elsevier Inc. All rights reserved.
  • (PMID = 19070941.001).
  • [ISSN] 1558-1497
  • [Journal-full-title] Neurobiology of aging
  • [ISO-abbreviation] Neurobiol. Aging
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II
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17. Pan XD, Chen XC, Zhu YG, Chen LM, Zhang J, Huang TW, Ye QY, Huang HP: Tripchlorolide protects neuronal cells from microglia-mediated beta-amyloid neurotoxicity through inhibiting NF-kappaB and JNK signaling. Glia; 2009 Aug 15;57(11):1227-38
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  • [Title] Tripchlorolide protects neuronal cells from microglia-mediated beta-amyloid neurotoxicity through inhibiting NF-kappaB and JNK signaling.
  • Recent research has focused on soluble oligomeric assemblies of beta-amyloid peptides (Abeta) as the proximate cause of neuroinflammation, synaptic loss, and the eventual dementia associated with Alzheimer's disease (AD).
  • T4 significantly attenuated oligomeric Abeta(1-42)-induced release of inflammatory productions such as tumor necrosis factor-alpha, interleukin-1beta, nitric oxide (NO), and prostaglandin E2.
  • [MeSH-major] Amyloid beta-Peptides / toxicity. Diterpenes / pharmacology. MAP Kinase Signaling System / drug effects. Microglia / drug effects. NF-kappa B p50 Subunit / metabolism. Neurons / drug effects. Neuroprotective Agents / pharmacology. Peptide Fragments / toxicity. Phenanthrenes / pharmacology

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  • (PMID = 19170180.001).
  • [ISSN] 1098-1136
  • [Journal-full-title] Glia
  • [ISO-abbreviation] Glia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Diterpenes; 0 / NF-kappa B p50 Subunit; 0 / Neuroprotective Agents; 0 / Peptide Fragments; 0 / Phenanthrenes; 0 / amyloid beta-protein (1-42); 132368-08-2 / tripchlorolide; 147257-52-1 / Nfkb1 protein, mouse; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases
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18. Shiels SA, Hasan SI, Darowski A: Collapse in a 79-year-old: a rare case of amyloid tumour of the pelvis. Age Ageing; 2005 Nov;34(6):648-9
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  • [Title] Collapse in a 79-year-old: a rare case of amyloid tumour of the pelvis.
  • Further investigations showed that the mass contained amyloid protein.
  • With no evidence of systemic amyloidosis or malignancy a diagnosis of amyloidoma/amyloid tumour was made.
  • This is the largest amyloid tumour reported in the literature to date.
  • Clearly amyloidomas are rare, but patients can present acutely and may have a poor prognosis, especially when the tumour is of considerable size.
  • [MeSH-major] Amyloid Neuropathies / complications. Leg. Lumbosacral Plexus. Pain / etiology. Pelvis

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  • (PMID = 16267196.001).
  • [ISSN] 0002-0729
  • [Journal-full-title] Age and ageing
  • [ISO-abbreviation] Age Ageing
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 10
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19. Lo BK, Yu M, Zloty D, Cowan B, Shapiro J, McElwee KJ: CXCR3/ligands are significantly involved in the tumorigenesis of basal cell carcinomas. Am J Pathol; 2010 May;176(5):2435-46
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  • [Title] CXCR3/ligands are significantly involved in the tumorigenesis of basal cell carcinomas.
  • Basal cell carcinoma (BCC) is the most common skin malignancy encountered worldwide.
  • We hypothesized that CXC chemokines, small cytokines involved in inducing directed leukocyte chemotaxis, could play a key role in the modulation of BCC growth.
  • In this study, quantitative RT-PCR revealed that the chemokines CXCL9, 10, 11, and their receptor CXCR3 were significantly upregulated by an average 22.6-fold, 9.2-fold, 26.6-fold, and 4.9-fold, respectively in BCC tissue samples as compared with nonlesional skin epithelium.
  • Immunohistochemistry analysis revealed that CXCR3, CXCL10, and CXCL11, but not CXCL9, colocalized with cytokeratin 17 (K17) in BCC keratinocytes.
  • In addition, CXCR3 and its ligands were expressed in cells of the surrounding BCC stroma.
  • The chemokines and K17 were also expressed in cultured human immortalized HaCaT keratinocytes.
  • Exposure of HaCaT cells or primary BCC-derived cells to CXCL11 peptides in vitro significantly increased cell proliferation.
  • In primary BCC-derived cell cultures, addition of CXCL11 progressively selected for K17+/CXCR3+ co-expressing cells over time.
  • The expression of CXCR3 and its ligands in human BCC keratinocytes, the enhancement of keratinocyte cell proliferation by CXCL11, and the homogeneity of K17+ BCC cells in human BCC-isolated cell population supported by CXCR3/CXCL11 signaling all suggest that CXCR3 and its ligands may be important autocrine and/or paracrine signaling mediators in the tumorigenesis of BCC.

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  • (PMID = 20228225.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / / MUS-94025
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CXCL11 protein, human; 0 / Chemokine CXCL11; 0 / Ligands; 0 / Receptors, CXCR3
  • [Other-IDs] NLM/ PMC2861108
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20. Kauf AC, Rosenbusch RF, Paape MJ, Bannerman DD: Innate immune response to intramammary Mycoplasma bovis infection. J Dairy Sci; 2007 Jul;90(7):3336-48
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  • Acute phase protein synthesis, which reflects 1 parameter of the systemic response to infection, was induced within 108 h of infection, as evidenced by increased circulating concentrations of lipopolysaccharide binding protein and serum amyloid A.
  • Milk concentrations of several cytokines, including IFN-gamma, IL-1beta, IL-10, IL-12, tumor growth factor-alpha, and tumor necrosis factor-alpha, were elevated in response to infection over a period of several days, whereas increases in milk IL-8 were of a more limited duration.

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  • (PMID = 17582119.001).
  • [ISSN] 1525-3198
  • [Journal-full-title] Journal of dairy science
  • [ISO-abbreviation] J. Dairy Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Serum Albumin; 0 / aflatoxin B1-bovine serum albumin; 80295-54-1 / Complement C5a; 9N2N2Y55MH / Aflatoxin B1
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21. Kerr ML, Gasperini R, Gibbs ME, Hou X, Shepherd CE, Strickland DK, Foa L, Lawen A, Small DH: Inhibition of Abeta aggregation and neurotoxicity by the 39-kDa receptor-associated protein. J Neurochem; 2010 Mar;112(5):1199-209
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  • Aggregation of beta-amyloid protein (Abeta) to form oligomers is considered to be a key step in generating neurotoxicity in the Alzheimer's disease brain.
  • [MeSH-major] Amyloid beta-Peptides / metabolism. LDL-Receptor Related Protein-Associated Protein / therapeutic use. Neurotoxicity Syndromes / drug therapy. Neurotoxicity Syndromes / metabolism
  • [MeSH-minor] Analysis of Variance. Animals. Animals, Newborn. Avoidance Learning / drug effects. Behavior, Animal. Cell Line, Tumor. Chickens. Discrimination Learning / drug effects. Disease Models, Animal. Flow Cytometry / methods. Fluorescein / metabolism. Humans. Immunoprecipitation / methods. Memory / drug effects. Microscopy, Atomic Force / methods. Microscopy, Confocal / methods. Molecular Weight. Neuroblastoma. Nuclear Proteins / metabolism. Peptide Fragments / metabolism. Peptide Fragments / pharmacology. Protein Binding. Protein Transport / drug effects

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  • (PMID = 20002523.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL50784; United States / NHLBI NIH HHS / HL / HL54710
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / LDL-Receptor Related Protein-Associated Protein; 0 / Nuclear Proteins; 0 / Peptide Fragments; 0 / amyloid beta-protein (1-40); 0 / amyloid beta-protein (1-42); TPY09G7XIR / Fluorescein
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22. Patel JR, Brewer GJ: Age-related differences in NFkappaB translocation and Bcl-2/Bax ratio caused by TNFalpha and Abeta42 promote survival in middle-age neurons and death in old neurons. Exp Neurol; 2008 Sep;213(1):93-100
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  • [Title] Age-related differences in NFkappaB translocation and Bcl-2/Bax ratio caused by TNFalpha and Abeta42 promote survival in middle-age neurons and death in old neurons.
  • Alzheimer's disease is associated with an age-related accumulation of Abeta and inflammation.
  • The inflammatory mediator, TNFalpha activates a signaling cascade involving NFkappaB translocation to the nucleus and a beneficial or detrimental transcriptional response, depending on the age of the neurons and the type of stress applied.
  • Relative to treatment with Abeta42 alone, previously we found that TNFalpha plus Abeta42, applied to old rat neurons (24 month) is toxic, while the same treatment of middle-age neurons (10 month) is protective.
  • In contrast to improved survival of middle-age rat cortical neurons, neurons from old rats are killed by TNFalpha plus Abeta42 despite greater p50 nuclear translocation.
  • In middle-age neurons, blocking TNFR1 does not affect NFkappaB translocation, whereas blocking TNFR2 results in an increase in NFkappaB translocation.
  • For old neurons, blocking either receptor, does not change NFkappaB translocation, but improves cell survival.
  • To account for these effects on cell viability in response to TNF+Abeta, measures of the Bcl-2/Bax ratio positively correlate with survival.
  • In the setting of old neurons, these results suggest that overactivated nuclear translocation of NFkappaB and lower Bcl-2 levels promote death that is reduced by inhibition of either TNFR1 or R2.

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  • (PMID = 18625500.001).
  • [ISSN] 1090-2430
  • [Journal-full-title] Experimental neurology
  • [ISO-abbreviation] Exp. Neurol.
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG013435-09; United States / NIA NIH HHS / AG / R01 AG013435; United States / NIA NIH HHS / AG / R01 AG013435-09
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / NF-kappa B; 0 / Peptide Fragments; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Tumor Necrosis Factor, Type I; 0 / Receptors, Tumor Necrosis Factor, Type II; 0 / Tnfrsf1a protein, rat; 0 / Tumor Necrosis Factor-alpha; 0 / amyloid beta-protein (1-42); 0 / bcl-2-Associated X Protein
  • [Other-IDs] NLM/ NIHMS68440; NLM/ PMC2597588
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23. Sharma VM, Calvo JA, Draheim KM, Cunningham LA, Hermance N, Beverly L, Krishnamoorthy V, Bhasin M, Capobianco AJ, Kelliher MA: Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-myc. Mol Cell Biol; 2006 Nov;26(21):8022-31
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  • [Title] Notch1 contributes to mouse T-cell leukemia by directly inducing the expression of c-myc.
  • Recent work with mouse models and human leukemic samples has shown that gain-of-function mutation(s) in Notch1 is a common genetic event in T-cell acute lymphoblastic leukemia (T-ALL).
  • The Notch1 receptor signals through a gamma-secretase-dependent process that releases intracellular Notch1 from the membrane to the nucleus, where it forms part of a transcriptional activator complex.
  • To identify Notch1 target genes in leukemia, we developed mouse T-cell leukemic lines that express intracellular Notch1 in a doxycycline-dependent manner.
  • Using gene expression profiling and chromatin immunoprecipitation, we identified c-myc as a novel, direct, and critical Notch1 target gene in T-cell leukemia. c-myc mRNA levels are increased in primary mouse T-cell tumors that harbor Notch1 mutations, and Notch1 inhibition decreases c-myc mRNA levels and inhibits leukemic cell growth.
  • Retroviral expression of c-myc, like intracellular Notch1, rescues the growth arrest and apoptosis associated with gamma-secretase inhibitor treatment or Notch1 inhibition.
  • Consistent with these findings, retroviral insertional mutagenesis screening of our T-cell leukemia mouse model revealed common insertions in either notch1 or c-myc genes.
  • These studies define the Notch1 molecular signature in mouse T-ALL and importantly provide mechanistic insight as to how Notch1 contributes to human T-ALL.

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  • (PMID = 16954387.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096899; United States / NCI NIH HHS / CA / CA-096889
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Enzyme Inhibitors; 0 / Myc protein, mouse; 0 / Notch1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myc; 0 / Receptor, Notch1; 0 / Tal1 protein, mouse; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC1636748
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24. Cantarella G, Di Benedetto G, Pezzino S, Risuglia N, Bernardini R: TRAIL-related neurotoxicity implies interaction with the Wnt pathway in human neuronal cells in vitro. J Neurochem; 2008 Jun;105(5):1915-23
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  • Tumor necrosis factor related apoptosis inducing ligand (TRAIL) is involved in amyloid beta dependent neurotoxicity via the extrinsic pathway.
  • Recently, several genes modulating TRAIL cytotoxicity have been characterized, providing evidence for a role of wingless-type mouse mammary tumor virus integration site family (Wnt), Jun-N-terminal kinase and other pathways in increased cell susceptibility to the cytokine.
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / physiology. Cell Line, Tumor. Humans

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  • (PMID = 18266928.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / Wnt Proteins
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25. Staropoli JF: Tumorigenesis and neurodegeneration: two sides of the same coin? Bioessays; 2008 Aug;30(8):719-27
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  • Increased dosage of amyloid precursor protein in Down syndrome (trisomy 21) predisposes to dementia of Alzheimer type and may also contribute to acute leukemia and transient myeloproliferative disorder.
  • The gene parkin, loss-of-function mutations in which account for about half of cases of early-onset Parkinson disease, has been identified as a candidate tumor suppressor gene by several groups.
  • Parkin is deleted or downregulated in several tumor types, and its re-expression sensitizes derivative cell lines to inhibitors of cell-cycle progression.
  • [MeSH-minor] Amyloid / metabolism. Animals. Ataxia Telangiectasia Mutated Proteins. Biomarkers / metabolism. Cell Cycle. Cell Cycle Proteins / metabolism. DNA-Binding Proteins / metabolism. Down Syndrome / genetics. Down Syndrome / pathology. Humans. Models, Biological. Mutation. Neurons / metabolism. Parkinson Disease / genetics. Parkinson Disease / pathology. Protein-Serine-Threonine Kinases / metabolism. Tumor Suppressor Proteins / metabolism

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  • [Copyright] (c) 2008 Wiley Periodicals, Inc.
  • (PMID = 18623069.001).
  • [ISSN] 1521-1878
  • [Journal-full-title] BioEssays : news and reviews in molecular, cellular and developmental biology
  • [ISO-abbreviation] Bioessays
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid; 0 / Biomarkers; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Number-of-references] 90
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26. Dong Y, Zhang G, Zhang B, Moir RD, Xia W, Marcantonio ER, Culley DJ, Crosby G, Tanzi RE, Xie Z: The common inhalational anesthetic sevoflurane induces apoptosis and increases beta-amyloid protein levels. Arch Neurol; 2009 May;66(5):620-31
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  • [Title] The common inhalational anesthetic sevoflurane induces apoptosis and increases beta-amyloid protein levels.
  • OBJECTIVE: To assess the effects of sevoflurane, the most commonly used inhalation anesthetic, on apoptosis and beta-amyloid protein (Abeta) levels in vitro and in vivo.
  • Subjects Naive mice, H4 human neuroglioma cells, and H4 human neuroglioma cells stably transfected to express full-length amyloid precursor protein.
  • INTERVENTIONS: Human H4 neuroglioma cells stably transfected to express full-length amyloid precursor protein were exposed to 4.1% sevoflurane for 6 hours.
  • RESULTS: Sevoflurane induced apoptosis and elevated levels of beta-site amyloid precursor protein-cleaving enzyme and Abeta in vitro and in vivo.
  • These results suggest that sevoflurane induces caspase activation which, in turn, enhances beta-site amyloid precursor protein-cleaving enzyme and Abeta levels.

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  • (PMID = 19433662.001).
  • [ISSN] 1538-3687
  • [Journal-full-title] Archives of neurology
  • [ISO-abbreviation] Arch. Neurol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / K08 NS048140-05; United States / NIA NIH HHS / AG / R21 AG029856; United States / NIA NIH HHS / AG / AG029856; United States / NINDS NIH HHS / NS / NS048140-05; United States / NINDS NIH HHS / NS / K08 NS048140-04; United States / NIGMS NIH HHS / GM / R01 GM088801; United States / NIGMS NIH HHS / GM / GM077507; United States / NIA NIH HHS / AG / AG2025; United States / NIA NIH HHS / AG / AG029856-01A2; United States / NINDS NIH HHS / NS / NS048140-04; United States / NINDS NIH HHS / NS / NS048140; United States / NINDS NIH HHS / NS / K08 NS048140; United States / NIGMS NIH HHS / GM / GM088801-01A1; United States / NIGMS NIH HHS / GM / R01 GM088801-01A1; United States / NIA NIH HHS / AG / R21 AG029856-01A2; United States / NIGMS NIH HHS / GM / GM088801
  • [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 / Amyloid beta-Peptides; 0 / Anesthetics, Inhalation; 0 / Enzyme Inhibitors; 0 / Methyl Ethers; 38LVP0K73A / sevoflurane; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS130512; NLM/ PMC2748878
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27. Clementz AG, Osipo C: Notch versus the proteasome: what is the target of gamma-secretase inhibitor-I? Breast Cancer Res; 2009;11(5):110
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Breast Neoplasms / drug therapy. Breast Neoplasms / enzymology. Receptors, Notch / antagonists & inhibitors
  • [MeSH-minor] Cell Line, Tumor. Female. Humans. Leupeptins / pharmacology. Oligopeptides / pharmacology

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  • [CommentOn] Breast Cancer Res. 2009;11(4):R57 [19660128.001]
  • (PMID = 19849815.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Leupeptins; 0 / Oligopeptides; 0 / Receptors, Notch; 0 / benzyloxycarbonyl-leucyl-leucyl-norleucinal; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ PMC2790851
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28. Behle JH, Sedaghatfar MH, Demmer RT, Wolf DL, Celenti R, Kebschull M, Belusko PB, Herrera-Abreu M, Lalla E, Papapanou PN: Heterogeneity of systemic inflammatory responses to periodontal therapy. J Clin Periodontol; 2009 Apr;36(4):287-94
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  • However, only sE-selectin, sICAM, and serum amyloid P sustained a reduction at T4.

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  • (PMID = 19426174.001).
  • [ISSN] 1600-051X
  • [Journal-full-title] Journal of clinical periodontology
  • [ISO-abbreviation] J. Clin. Periodontol.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / K99 DE-018739; United States / NIDCR NIH HHS / DE / DE015649-03; United States / NIDCR NIH HHS / DE / DE015649-02; United States / NIDCR NIH HHS / DE / R01 DE015649-03; United States / NIDCR NIH HHS / DE / DE015649; United States / NIDCR NIH HHS / DE / R01 DE015649; United States / NIDCR NIH HHS / DE / K99 DE018739; United States / NIDCR NIH HHS / DE / R01 DE015649-02
  • [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 / Adiponectin; 0 / Antibodies, Bacterial; 0 / E-Selectin; 0 / Inflammation Mediators; 0 / Interleukins; 0 / Plasminogen Activator Inhibitor 1; 0 / Serum Amyloid P-Component; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; 9007-41-4 / C-Reactive Protein; EC 1.11.1.7 / Peroxidase; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ NIHMS133569; NLM/ PMC2753407
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29. Saruc M, Iki K, Pour PM: Morphometric studies in human pancreatic cancer argues against the etiological role of type 2 diabetes in pancreatic cancer. Histol Histopathol; 2010 04;25(4):423-32
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  • BACKGROUND: To understand the role of islet amyloid polypeptide (IAPP) in type 2 diabetes and pancreatic cancer (PC), we investigated the patterns of its expression and its ratio to insulin, glucagon, somatostatin and pancreatic polypeptide cells by morphometry in tissues from these two diseases in comparison to the normal pancreas.
  • MATERIALS AND METHODS: Pancreatic tissues from 11 donors (five without pancreatic disease and six with type 2 diabetes) and 11 surgical specimens from PC patients obtained from the cancer area (zone A) and the adjacent tumor-free area (zone B) were examined immunohistochemically.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Amyloid / metabolism. Biomarkers, Tumor / metabolism. Female. Glucagon / metabolism. Humans. Immunoenzyme Techniques. Insulin / metabolism. Islet Amyloid Polypeptide. Islets of Langerhans / metabolism. Islets of Langerhans / pathology. Male. Middle Aged. Pancreatic Polypeptide / metabolism


30. Qi XL, Shan KR, Xiao Y, Liu RY, Gu R, Guan ZZ: [Influence of beta-amyloid peptide on cell membrane lipids and cholinergic receptors in human neuroblastoma SH-SY5Y cells]. Zhonghua Bing Li Xue Za Zhi; 2006 Jan;35(1):37-41
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  • [Title] [Influence of beta-amyloid peptide on cell membrane lipids and cholinergic receptors in human neuroblastoma SH-SY5Y cells].
  • OBJECTIVE: To study the effects of beta-amyloid peptide (Abeta) on cell membrane lipids and cholinergic receptors of human neuroblastoma cells.
  • CONCLUSION: beta-amyloid peptide reduces the level of cell membrane lipids and cholinergic receptors in human SH-SY5Y neuroblastoma cells, likely through the induction of an enhanced oxidative stress.
  • [MeSH-major] Amyloid beta-Peptides / toxicity. Membrane Lipids / metabolism. Neuroblastoma / metabolism. Peptide Fragments / toxicity. Receptors, Nicotinic / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Membrane / metabolism. Cholesterol / metabolism. Dose-Response Relationship, Drug. Humans. Lipid Peroxidation / drug effects. Malondialdehyde / metabolism. Oxidative Stress / drug effects. Phospholipids / metabolism. Ubiquinone / metabolism. Vitamin E / metabolism. Vitamin E / pharmacology

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  • (PMID = 16608648.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Membrane Lipids; 0 / Peptide Fragments; 0 / Phospholipids; 0 / Receptors, Nicotinic; 0 / amyloid beta-protein (1-42); 0 / nicotinic receptor subunit alpha3; 1339-63-5 / Ubiquinone; 1406-18-4 / Vitamin E; 4Y8F71G49Q / Malondialdehyde; 97C5T2UQ7J / Cholesterol
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31. Billion K, Ibrahim H, Mauch C, Niessen CM: Increased soluble E-cadherin in melanoma patients. Skin Pharmacol Physiol; 2006;19(2):65-70
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  • However, we did find a significant increase in serum E-cadherin levels of melanoma patients with advanced disease correlating with increased S100 tumor marker values, suggesting that increased cadherin shedding may contribute to melanoma progression.
  • [MeSH-minor] Amyloid Precursor Protein Secretases. Aspartic Acid Endopeptidases. Blotting, Western. Cell Line, Tumor. Endopeptidases / metabolism. Humans. S100 Proteins / metabolism

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  • [Copyright] Copyright 2006 S. Karger AG, Basel.
  • (PMID = 16685144.001).
  • [ISSN] 1660-5527
  • [Journal-full-title] Skin pharmacology and physiology
  • [ISO-abbreviation] Skin Pharmacol Physiol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cadherins; 0 / S100 Proteins; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.- / Endopeptidases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human
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32. Yang L, Hao J, Zhang J, Xia W, Dong X, Hu X, Kong F, Cui X: Ginsenoside Rg3 promotes beta-amyloid peptide degradation by enhancing gene expression of neprilysin. J Pharm Pharmacol; 2009 Mar;61(3):375-80
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  • [Title] Ginsenoside Rg3 promotes beta-amyloid peptide degradation by enhancing gene expression of neprilysin.
  • OBJECTIVES: It has been hypothesized that the accumulation of beta-amyloid peptide (Abeta) in the brain is a triggering event leading to the pathological cascade of Alzheimer's disease.
  • METHODS: In this study, we investigated the effect of ginsenoside Rg3, one of the major active components of ginseng, on the metabolism of Abeta40 and Abeta42 in SK-N-SH cells transfected with Swedish mutant beta-amyloid precursor protein (SweAPP).
  • [MeSH-major] Amyloid beta-Peptides / drug effects. Ginsenosides / pharmacology. Neprilysin / drug effects. Peptide Fragments / drug effects
  • [MeSH-minor] Alzheimer Disease / drug therapy. Alzheimer Disease / physiopathology. Blotting, Western. Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. Gene Expression Regulation / drug effects. Humans. Medicine, Chinese Traditional. Neuroblastoma / metabolism. Panax / chemistry. Polymerase Chain Reaction. Transfection

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  • (PMID = 19222911.001).
  • [ISSN] 0022-3573
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Ginsenosides; 0 / Peptide Fragments; 0 / amyloid beta-protein (1-40); 0 / amyloid beta-protein (1-42); 14197-60-5 / ginsenoside Rg3; EC 3.4.24.11 / Neprilysin
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33. Dowling P, O'Driscoll L, Meleady P, Henry M, Roy S, Ballot J, Moriarty M, Crown J, Clynes M: 2-D difference gel electrophoresis of the lung squamous cell carcinoma versus normal sera demonstrates consistent alterations in the levels of ten specific proteins. Electrophoresis; 2007 Dec;28(23):4302-10
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  • Proteins found to have increased abundance levels in squamous cell carcinoma sera compared to normal sera included apolipoprotein A-IV precursor, chain F; human complement component C3c, haptoglobin, serum amyloid A protein precursor and Ras-related protein Rab-7b.
  • [MeSH-major] Biomarkers, Tumor / blood. Blood Proteins / analysis. Carcinoma, Squamous Cell / blood. Electrophoresis, Gel, Two-Dimensional / methods. Lung Neoplasms / blood. Mass Spectrometry / methods

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  • (PMID = 18041032.001).
  • [ISSN] 0173-0835
  • [Journal-full-title] Electrophoresis
  • [ISO-abbreviation] Electrophoresis
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Validation Studies
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Blood Proteins; 0 / Haptoglobins
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34. Papassotiriou I, Alexiou VG, Tsironi M, Skenderi K, Spanos A, Falagas ME: Severe aseptic inflammation caused by long distance running (246 km) does not increase procalcitonin. Eur J Clin Invest; 2008 Apr;38(4):276-9
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  • Serum interleukin-6, serum amyloid A protein, C-reactive protein, tumour necrosis factor-alpha and procalcitonin concentrations were determined.
  • RESULTS: Serum interleukin-6, serum amyloid A protein and C-reactive protein were dramatically increased after the end of the race (150-, 116- and 10,470- fold increase of the mean values, respectively).
  • Tumour necrosis factor-alpha measurements revealed no significant changes.
  • [MeSH-minor] Adult. Humans. Interleukin-6 / metabolism. Middle Aged. Serum Amyloid A Protein / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • [CommentIn] Eur J Clin Invest. 2008 Oct;38(10):784-5 [18837805.001]
  • (PMID = 18339008.001).
  • [ISSN] 1365-2362
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Protein Precursors; 0 / Serum Amyloid A Protein; 0 / Tumor Necrosis Factor-alpha; 56645-65-9 / procalcitonin; 9007-12-9 / Calcitonin; 9007-41-4 / C-Reactive Protein
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35. Tsai SJ, Lin CY, Mong MC, Ho MW, Yin MC: s-Ethyl cysteine and s-propyl cysteine alleviate beta-amyloid induced cytotoxicity in nerve growth factor differentiated PC12 cells. J Agric Food Chem; 2010 Jun 9;58(11):7104-8
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  • [Title] s-Ethyl cysteine and s-propyl cysteine alleviate beta-amyloid induced cytotoxicity in nerve growth factor differentiated PC12 cells.
  • Beta-amyloid peptide (Abeta) was used to induce cytotoxicity in nerve growth factor differentiated PC12 cells, and the effects of s-ethyl cysteine (SEC) and s-propyl cysteine (SPC) on anti-inflammatory protection, DNA fragmentation, mitochondrial membrane potential (MMP), and activity of Na(+)-K(+)-ATPase and caspases were examined.
  • Abeta treatment increased the protein production and mRNA expression of interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha (P < 0.05).
  • [MeSH-major] Alzheimer Disease / physiopathology. Amyloid beta-Peptides / toxicity. Cell Differentiation / drug effects. Cysteine / analogs & derivatives. Nerve Growth Factor / pharmacology

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  • (PMID = 20443605.001).
  • [ISSN] 1520-5118
  • [Journal-full-title] Journal of agricultural and food chemistry
  • [ISO-abbreviation] J. Agric. Food Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Neuroprotective Agents; 2139-90-4 / S-ethylcysteine; 65309-79-7 / S-propylcysteine; 9061-61-4 / Nerve Growth Factor; K848JZ4886 / Cysteine
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36. Kam AY, Tse TT, Kwan DH, Wong YH: Formyl peptide receptor like 1 differentially requires mitogen-activated protein kinases for the induction of glial fibrillary acidic protein and interleukin-1alpha in human U87 astrocytoma cells. Cell Signal; 2007 Oct;19(10):2106-17
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  • [MeSH-minor] Amyloid beta-Peptides / toxicity. Animals. Astrocytoma. CHO Cells. Cell Death. Cell Line, Tumor. Cricetinae. Cricetulus. Enzyme Inhibitors / pharmacology. GTP-Binding Protein alpha Subunits, Gi-Go / metabolism. Humans. Oligopeptides / pharmacology. Peptide Fragments / toxicity. Up-Regulation. src-Family Kinases / metabolism

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  • (PMID = 17643960.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Enzyme Inhibitors; 0 / FPR2 protein, human; 0 / Glial Fibrillary Acidic Protein; 0 / Interleukin-1alpha; 0 / Oligopeptides; 0 / Peptide Fragments; 0 / Receptors, Formyl Peptide; 0 / Receptors, Lipoxin; 0 / Trp-Lys-Tyr-Met-Val-Met; 0 / amyloid beta-protein (1-42); EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go
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37. Iribarren P, Chen K, Hu J, Zhang X, Gong W, Wang JM: IL-4 inhibits the expression of mouse formyl peptide receptor 2, a receptor for amyloid beta1-42, in TNF-alpha-activated microglia. J Immunol; 2005 Nov 1;175(9):6100-6
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  • [Title] IL-4 inhibits the expression of mouse formyl peptide receptor 2, a receptor for amyloid beta1-42, in TNF-alpha-activated microglia.
  • We have previously shown that TNF-alpha up-regulated the expression of formyl peptide receptor 2 (mFPR2) in mouse microglial cells, resulting in increased chemotactic responses of such cells to mFPR2 agonists, including amyloid beta1-42 (Abeta42), a critical pathogenic agent in Alzheimer's disease.
  • [MeSH-major] Amyloid beta-Peptides / metabolism. Interleukin-4 / pharmacology. Microglia / metabolism. Peptide Fragments / metabolism. Receptors, Formyl Peptide / antagonists & inhibitors. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 16237106.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / NF-kappa B; 0 / Peptide Fragments; 0 / Receptors, Formyl Peptide; 0 / STAT6 Transcription Factor; 0 / Tumor Necrosis Factor-alpha; 0 / amyloid beta-protein (1-42); 0 / formyl peptide receptor 2, mouse; 207137-56-2 / Interleukin-4; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.1.3.16 / Phosphoprotein Phosphatases; EC 3.1.3.16 / Protein Phosphatase 2
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38. Akiyoshi T, Nakamura M, Yanai K, Nagai S, Wada J, Koga K, Nakashima H, Sato N, Tanaka M, Katano M: Gamma-secretase inhibitors enhance taxane-induced mitotic arrest and apoptosis in colon cancer cells. Gastroenterology; 2008 Jan;134(1):131-44
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  • BACKGROUND & AIMS: Colorectal cancers are resistant to conventional chemotherapeutic treatments, including taxanes. gamma-Secretase is a multimeric membrane protein complex responsible for the intramembrane proteolysis of various type I transmembrane proteins, including amyloid beta-precursor protein and Notch. gamma-Secretase inhibitors have attracted increasing interest as anticancer drugs because of their ability to inhibit Notch signaling.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Apoptosis / drug effects. Colonic Neoplasms / pathology. Enzyme Inhibitors / pharmacology. Mitosis / drug effects
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Bridged Compounds / pharmacology. Cell Culture Techniques. Cell Line, Tumor. Humans. Taxoids / pharmacology. Vincristine / pharmacology

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  • (PMID = 18166351.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Bridged Compounds; 0 / Enzyme Inhibitors; 0 / Taxoids; 1605-68-1 / taxane; 5J49Q6B70F / Vincristine; EC 3.4.- / Amyloid Precursor Protein Secretases
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39. Yerbury JJ, Wilson MR: Extracellular chaperones modulate the effects of Alzheimer's patient cerebrospinal fluid on Abeta(1-42) toxicity and uptake. Cell Stress Chaperones; 2010 Jan;15(1):115-21
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  • [MeSH-major] Alzheimer Disease / cerebrospinal fluid. Amyloid beta-Peptides / toxicity. Molecular Chaperones / pharmacology. Peptide Fragments / toxicity
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Line, Tumor. Humans. Male. Microscopy, Fluorescence. Middle Aged. Protein Binding

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  • (PMID = 19472074.001).
  • [ISSN] 1466-1268
  • [Journal-full-title] Cell stress & chaperones
  • [ISO-abbreviation] Cell Stress Chaperones
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Molecular Chaperones; 0 / Peptide Fragments; 0 / amyloid beta-protein (1-42)
  • [Other-IDs] NLM/ PMC2866977
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40. Sevimli A, Misirlioğlu D, Yağci A, Bülbül A, Yilmaztepe A, Altunbas K: The role of chicken IL-1beta, IL-6 and TNF-alpha in the occurrence of amyloid arthropathy. Vet Res Commun; 2008 Oct;32(7):499-508
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  • [Title] The role of chicken IL-1beta, IL-6 and TNF-alpha in the occurrence of amyloid arthropathy.
  • In this study, the roles of IL-1beta, IL-6 and TNF-alpha in amyloid arthropathic chickens with variable amounts (severe, moderate and mild) of amyloid accumulation were investigated.
  • One hundred brown layer chicks were allocated into four groups and intra-articular injections of Freund's adjuvant were used to induce amyloid arthropathy in Groups II, III and IV.
  • At the end of the study, a positive correlation was observed among the incidence and severity of amyloidosis, the serum amyloid A levels and the IL-1beta values both in the serum and tissues.
  • [MeSH-major] Amyloidosis / veterinary. Interleukin-1beta / metabolism. Interleukin-6 / metabolism. Joint Diseases / veterinary. Poultry Diseases / metabolism. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18612836.001).
  • [ISSN] 0165-7380
  • [Journal-full-title] Veterinary research communications
  • [ISO-abbreviation] Vet. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha
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41. Uberti D, Cenini G, Olivari L, Ferrari-Toninelli G, Porrello E, Cecchi C, Pensalfini A, Liguri G, Govoni S, Racchi M, Maurizio M: Over-expression of amyloid precursor protein in HEK cells alters p53 conformational state and protects against doxorubicin. J Neurochem; 2007 Oct;103(1):322-33
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  • [Title] Over-expression of amyloid precursor protein in HEK cells alters p53 conformational state and protects against doxorubicin.
  • Here we show that human embryonic kidney (HEK) cells stably transfected with amyloid precursor protein (HEK-APP), expressed a conformational mutant-like and transcriptionally inactive p53 isoform, and turned out to be less sensitive to the cytotoxin doxorubicin in comparison with untransfected cells.
  • Changes in p53 conformational state and reduced sensitivity to doxorubicin were also found in untransfected HEK cells after exposure to nanomolar concentrations of beta-amyloid (Abeta) and these effects were antagonized by vitamin E.
  • [MeSH-major] Amyloid beta-Protein Precursor / biosynthesis. Doxorubicin / pharmacology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Amyloid beta-Peptides / metabolism. Amyloid beta-Peptides / pharmacology. Antineoplastic Agents / pharmacology. Cell Line. Humans. Kidney / cytology. Kidney / drug effects. Kidney / metabolism. Peptide Fragments / metabolism. Peptide Fragments / pharmacology. Protein Conformation / drug effects. Protein Folding. Vitamin E / pharmacology

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  • [ErratumIn] J Neurochem. 2008 Mar; 104(5) 1430. Pensafini, Anna [corrected to Pensalfini, Anna]
  • (PMID = 17608641.001).
  • [ISSN] 0022-3042
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Amyloid beta-Protein Precursor; 0 / Antineoplastic Agents; 0 / Peptide Fragments; 0 / Tumor Suppressor Protein p53; 0 / amyloid beta-protein (1-40); 0 / amyloid beta-protein (1-42); 1406-18-4 / Vitamin E; 80168379AG / Doxorubicin
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42. Morel M, Couturier J, Pontcharraud R, Gil R, Fauconneau B, Paccalin M, Page G: Evidence of molecular links between PKR and mTOR signalling pathways in Abeta neurotoxicity: role of p53, Redd1 and TSC2. Neurobiol Dis; 2009 Oct;36(1):151-61
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  • This study analysed the crosslink between the up regulation of double-stranded RNA-dependent-protein kinase (PKR) and the down regulation of mammalian target of rapamycin (mTOR) signalling pathways via p53, the protein Regulated in the Development and DNA damage response 1 (Redd1) and the tuberous sclerosis complex (TSC2) factors in two beta-amyloid peptide (Abeta) neurotoxicity models.
  • [MeSH-major] Amyloid beta-Peptides / toxicity. Neurons / drug effects. Peptide Fragments / toxicity. Protein Kinases / metabolism. Signal Transduction / drug effects. Tumor Suppressor Proteins / metabolism. eIF-2 Kinase / metabolism
  • [MeSH-minor] Analysis of Variance. Animals. Cell Nucleus / drug effects. Cell Nucleus / metabolism. Cells, Cultured. Cerebral Cortex / cytology. Cytoplasm / drug effects. Cytoplasm / metabolism. Embryo, Mammalian. Gene Expression Regulation / drug effects. Gene Expression Regulation / genetics. Humans. Immunoprecipitation / methods. Neuroblastoma / pathology. Phosphorylation / drug effects. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Rats. Rats, Wistar. Repressor Proteins / genetics. Repressor Proteins / metabolism. TOR Serine-Threonine Kinases. Transfection / methods. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 19631745.001).
  • [ISSN] 1095-953X
  • [Journal-full-title] Neurobiology of disease
  • [ISO-abbreviation] Neurobiol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Peptide Fragments; 0 / RNA, Small Interfering; 0 / RTP801 protein, rat; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / amyloid beta-protein (1-42); 4JG2LF96VF / tuberous sclerosis complex 2 protein; 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, rat; EC 2.7.11.1 / eIF-2 Kinase
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43. Laforga JB, Aranda FI: Pseudoangiosarcomatous features in medullary thyroid carcinoma spindle-cell variant. Report of a case studied by FNA and immunohistochemistry. Diagn Cytopathol; 2007 Jul;35(7):424-8
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  • Microscopically, the tumor exhibited spindle-cell pattern intermingled with a striking angiosarcoma-like pattern characterized by the presence of abortive lumen and clefts containing erythrocytes.
  • Dense hyaline extracellular amyloid was present.
  • The tumor cells were strongly positive for cytokeratin, chromogranine-A, synaptophysine, serotonin, calcitonin, and CEA.
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Diagnosis, Differential. Hemangiosarcoma / pathology. Humans. Male

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  • (PMID = 17580345.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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44. La Merrill M, Gordon RR, Hunter KW, Threadgill DW, Pomp D: Dietary fat alters pulmonary metastasis of mammary cancers through cancer autonomous and non-autonomous changes in gene expression. Clin Exp Metastasis; 2010 Feb;27(2):107-16
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  • Despite the substantial dietary impact on metastasis and its interaction with metastasis modifiers, HFD significantly altered the expression of only five genes in mammary tumors; four of which, including serum amyloid A (Saa), are downstream of the tumor suppressor PTEN.
  • Conversely, HFD altered the expression of 211 hepatic genes in a set of tumor free F2 control mice.
  • Independent of diet, pulmonary metastasis virulence correlates with mammary tumor expression of genes involved in endocrine cancers, inflammation, angiogenesis, and invasion.
  • These data support the existence of diet-dependent and independent cancer modifier networks underlying differential susceptibility to mammary cancer metastasis and suggest that diet influences cancer metastasis virulence through tumor autonomous and non-autonomous mechanisms.

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  • (PMID = 20151316.001).
  • [ISSN] 1573-7276
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / 5T32 HD049311; United States / NIDDK NIH HHS / DK / DK056350; United States / NIEHS NIH HHS / ES / T32ES007126; United States / NCI NIH HHS / CA / U01CA105417; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / BTN1A1 protein, human; 0 / Btn1a1 protein, mouse; 0 / Butyrophilins; 0 / Dietary Fats; 0 / Membrane Glycoproteins
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45. Jimenez Del Rio M, Velez-Pardo C: Insulin-like growth factor-1 prevents Abeta[25-35]/(H2O2)- induced apoptosis in lymphocytes by reciprocal NF-kappaB activation and p53 inhibition via PI3K-dependent pathway. Growth Factors; 2006 Mar;24(1):67-78
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Amyloid beta-Peptides / physiology. Apoptosis. Hydrogen Peroxide / metabolism. Insulin-Like Growth Factor I / physiology. Lymphocytes / physiology. NF-kappa B / metabolism. Peptide Fragments / physiology. Phosphatidylinositol 3-Kinases / metabolism. Tumor Suppressor Protein p53 / antagonists & inhibitors

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  • (PMID = 16393695.001).
  • [ISSN] 0897-7194
  • [Journal-full-title] Growth factors (Chur, Switzerland)
  • [ISO-abbreviation] Growth Factors
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Benzothiazoles; 0 / Chromones; 0 / Morpholines; 0 / NF-kappa B; 0 / Peptide Fragments; 0 / Thiazoles; 0 / Thiocarbamates; 0 / Tumor Suppressor Protein p53; 0 / amyloid beta-protein (25-35); 0 / pifithrin; 135467-92-4 / prolinedithiocarbamate; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 3FPU23BG52 / Toluene; 67763-96-6 / Insulin-Like Growth Factor I; 9DLQ4CIU6V / Proline; BBX060AN9V / Hydrogen Peroxide; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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46. Kip KE, Marroquin OC, Shaw LJ, Arant CB, Wessel TR, Olson MB, Johnson BD, Mulukutla S, Sopko G, Merz CN, Reis SE: Global inflammation predicts cardiovascular risk in women: a report from the Women's Ischemia Syndrome Evaluation (WISE) study. Am Heart J; 2005 Nov;150(5):900-6
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  • METHODS: From the WISE study, 580 women with fasting plasma samples of inflammatory markers (interleukin [IL]-6, IL-18, tumor necrosis factor alpha, transforming growth factor beta, CRP, serum amyloid A [SAA], and intercellular adhesion molecules) were analyzed over a median of 4.7 years follow-up.
  • RESULTS: In factor analysis, a "proinflammation" factor (cluster) loaded on IL-6, CRP, and SAA (r = 0.63-0.87); a "proinflammation and anti-inflammation" cluster loaded on IL-18 and tumor necrosis factor alpha (r = 0.72, 0.77); and an "immunosuppressive" factor loaded singly on transforming growth factor beta (r = 0.96).

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  • (PMID = 16290958.001).
  • [ISSN] 1097-6744
  • [Journal-full-title] American heart journal
  • [ISO-abbreviation] Am. Heart J.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HV / N01-HV-68161; United States / NHLBI NIH HHS / HV / N01-HV-68162; United States / NHLBI NIH HHS / HV / N01-HV-68163; United States / NHLBI NIH HHS / HV / N01-HV-68164; United States / NHLBI NIH HHS / HL / R01-HL-073412-01; United States / NHLBI NIH HHS / HL / U01 HL649141; United States / NHLBI NIH HHS / HL / U01 HL649241; United States / PHS HHS / / U0164829
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Inflammation Mediators
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47. Nehar S, Mishra M, Heese K: Identification and characterisation of the novel amyloid-beta peptide-induced protein p17. FEBS Lett; 2009 Oct 6;583(19):3247-53
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  • [Title] Identification and characterisation of the novel amyloid-beta peptide-induced protein p17.
  • Amyloid-beta peptide (Abeta) achieves neurodegeneration through unknown mechanisms.
  • It impedes survival factors and enhances amyloid precursor protein expression thus suggesting its involvement in the Abeta-mediated pro-apoptotic pathways in AD.
  • [MeSH-major] Alzheimer Disease / metabolism. Alzheimer Disease / pathology. Amyloid beta-Peptides / metabolism. Apoptosis. Apoptosis Regulatory Proteins / metabolism. Peptide Fragments / metabolism
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Line, Tumor. Disease Models, Animal. Humans. Mice. Molecular Sequence Data. Rats. Tissue Distribution


48. Gopalakrishnan R, Simonton S, Rohrer MD, Koutlas IG: Cystic variant of calcifying epithelial odontogenic tumor. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2006 Dec;102(6):773-7
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  • [Title] Cystic variant of calcifying epithelial odontogenic tumor.
  • Calcifying epithelial odontogenic tumor (CEOT) is a benign, locally aggressive odontogenic neoplasm characterized by sheets and nests of epithelial cells with deeply eosinophilic or occasionally clear cytoplasm, calcifications, and eosinophilic amorphous material that stains positive for amyloid.

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  • (PMID = 17138180.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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49. Costantini C, Weindruch R, Della Valle G, Puglielli L: A TrkA-to-p75NTR molecular switch activates amyloid beta-peptide generation during aging. Biochem J; 2005 Oct 1;391(Pt 1):59-67
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  • [Title] A TrkA-to-p75NTR molecular switch activates amyloid beta-peptide generation during aging.
  • The abnormal accumulation of Abeta (amyloid beta-peptide) in the form of senile plaques is one of the main characteristics of AD.
  • In the present study, we show that two members of the neurotrophin receptor superfamily, TrkA (tyrosine kinase receptor A) and p75NTR (p75 neurotrophin receptor), differentially regulate the processing of APP (amyloid precursor protein): TrkA reduces, whereas p75NTR activates, beta-cleavage of APP.

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  • (PMID = 15966860.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS045669; United States / NINDS NIH HHS / NS / NS045669
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Ceramides; 0 / Polyenes; 0 / Polyunsaturated Alkamides; 0 / Receptor, Nerve Growth Factor; 52665-74-4 / manumycin; EC 2.7.10.1 / Receptor, trkA
  • [Other-IDs] NLM/ PMC1237139
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50. Schmid K, Haslbeck M, Buchner J, Somoza V: Induction of heat shock proteins and the proteasome system by casein-N epsilon-(carboxymethyl)lysine and N epsilon-(carboxymethyl)lysine in Caco-2 cells. Ann N Y Acad Sci; 2008 Apr;1126:257-61
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  • Exposure of Caco-2 cells to beta-amyloid, a nonglycation product, revealed similar results.
  • [MeSH-minor] Adenocarcinoma / metabolism. Blotting, Western. Cell Line, Tumor. Colonic Neoplasms / metabolism. Humans. Mass Spectrometry. Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

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  • (PMID = 18448826.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caseins; 0 / Glycosylation End Products, Advanced; 5746-04-3 / N(6)-carboxymethyllysine; K3Z4F929H6 / Lysine
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51. Wen Y, Yu WH, Maloney B, Bailey J, Ma J, Marié I, Maurin T, Wang L, Figueroa H, Herman M, Krishnamurthy P, Liu L, Planel E, Lau LF, Lahiri DK, Duff K: Transcriptional regulation of beta-secretase by p25/cdk5 leads to enhanced amyloidogenic processing. Neuron; 2008 Mar 13;57(5):680-90
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  • [Title] Transcriptional regulation of beta-secretase by p25/cdk5 leads to enhanced amyloidogenic processing.
  • Cyclin-dependent kinase 5 (cdk5) has been implicated in Alzheimer's disease (AD) pathogenesis.
  • Here, we demonstrate that overexpression of p25, an activator of cdk5, led to increased levels of BACE1 mRNA and protein in vitro and in vivo.
  • A p25/cdk5 responsive region containing multiple sites for signal transducer and activator of transcription (STAT1/3) was identified in the BACE1 promoter.
  • STAT3 interacts with the BACE1 promoter, and p25-overexpressing mice had elevated levels of pSTAT3 and BACE1, whereas cdk5-deficient mice had reduced levels.
  • Furthermore, mice with a targeted mutation in the STAT3 cdk5 responsive site had lower levels of BACE1.
  • Increased BACE levels in p25 overexpressing mice correlated with enhanced amyloidogenic processing that could be reversed by a cdk5 inhibitor.
  • These data demonstrate a pathway by which p25/cdk5 increases the amyloidogenic processing of APP through STAT3-mediated transcriptional control of BACE1 that could have implications for AD pathogenesis.

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  • (PMID = 18341989.001).
  • [ISSN] 1097-4199
  • [Journal-full-title] Neuron
  • [ISO-abbreviation] Neuron
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / AG18379; United States / NIA NIH HHS / AG / R01 AG018884; United States / NIA NIH HHS / AG / P01 AG017216-020004; United States / NINDS NIH HHS / NS / NS48447; United States / NIA NIH HHS / AG / AG017216-020004; United States / NINDS NIH HHS / NS / P01 NS048447; United States / NINDS NIH HHS / NS / NS048447-030005; United States / NIA NIH HHS / AG / AG18884; United States / NINDS NIH HHS / NS / P01 NS048447-030005; United States / NIA NIH HHS / AG / P01 AG017216; United States / NIA NIH HHS / AG / R01 AG018379; United States / NIA NIH HHS / AG / AG172116
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Amyloid beta-Protein Precursor; 0 / Cdk5r1 protein, mouse; 0 / Nerve Tissue Proteins; EC 2.7.- / Phosphotransferases; EC 2.7.11.22 / Cyclin-Dependent Kinase 5; EC 3.4.- / Amyloid Precursor Protein Secretases
  • [Other-IDs] NLM/ NIHMS43369; NLM/ PMC2329816
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52. Kusaka T, Ueno M, Miki T, Kanenishi K, Nagai Y, Huang CL, Okamoto Y, Ogawa T, Onodera M, Itoh S, Akiguchi I, Sakamoto H: Accumulation of triosephosphate isomerase, with sequence homology to Beta amyloid peptides, in vessel walls of the newborn piglet hippocampus. Microsc Res Tech; 2007 Jul;70(7):648-55
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  • [Title] Accumulation of triosephosphate isomerase, with sequence homology to Beta amyloid peptides, in vessel walls of the newborn piglet hippocampus.
  • We investigated whether beta-amyloid (Abeta)-like immunoreactivity was seen in the brains of newborn piglets.
  • It was colocalized with immunoreactivity for receptor for advanced glycation end product and tumor necrosis factor-alpha.
  • [MeSH-major] Amyloid beta-Peptides / chemistry. Blood Vessels / enzymology. Hippocampus / blood supply. Hippocampus / enzymology. Triose-Phosphate Isomerase / chemistry. Triose-Phosphate Isomerase / metabolism

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  • (PMID = 17393492.001).
  • [ISSN] 1059-910X
  • [Journal-full-title] Microscopy research and technique
  • [ISO-abbreviation] Microsc. Res. Tech.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; EC 5.3.1.1 / Triose-Phosphate Isomerase
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53. Ristorcelli E, Beraud E, Mathieu S, Lombardo D, Verine A: Essential role of Notch signaling in apoptosis of human pancreatic tumoral cells mediated by exosomal nanoparticles. Int J Cancer; 2009 Sep 1;125(5):1016-26
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  • [MeSH-minor] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Basic Helix-Loop-Helix Transcription Factors / genetics. Basic Helix-Loop-Helix Transcription Factors / metabolism. Blotting, Western. Carbamates / pharmacology. Caspase 3 / metabolism. Cell Differentiation. Cell Proliferation. Dipeptides / pharmacology. Flow Cytometry. Glycogen Synthase Kinase 3 / genetics. Glycogen Synthase Kinase 3 / metabolism. Homeodomain Proteins / genetics. Homeodomain Proteins / metabolism. Humans. Mitochondria / metabolism. PTEN Phosphohydrolase / genetics. PTEN Phosphohydrolase / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • [Copyright] 2009 UICC.
  • (PMID = 19405120.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Carbamates; 0 / Dipeptides; 0 / Homeodomain Proteins; 0 / L 685458; 0 / RNA, Messenger; 0 / Receptors, Notch; 149348-15-2 / HES1 protein, human; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.22.- / Caspase 3
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54. Choi SC, Choi EJ, Oh HM, Lee S, Lee JK, Lee MS, Shin YI, Choi SJ, Chae JR, Lee KM, Lee WJ, Park JS, Shin CY, Oh TY, Jun CD: DA-9601, a standardized extract of Artemisia asiatica, blocks TNF-alpha-induced IL-8 and CCL20 production by inhibiting p38 kinase and NF-kappaB pathways in human gastric epithelial cells. World J Gastroenterol; 2006 Aug 14;12(30):4850-8
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  • [MeSH-major] Chemokines, CC / metabolism. Epithelial Cells / metabolism. Interleukin-8 / metabolism. Macrophage Inflammatory Proteins / metabolism. NF-kappa B / antagonists & inhibitors. Plant Extracts / pharmacology. Tumor Necrosis Factor-alpha / metabolism. p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors

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  • (PMID = 16937467.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / CCL20 protein, human; 0 / Chemokine CCL20; 0 / Chemokines, CC; 0 / DA 9601; 0 / Enzyme Inhibitors; 0 / Interleukin-8; 0 / Macrophage Inflammatory Proteins; 0 / NF-kappa B; 0 / Plant Extracts; 0 / Tumor Necrosis Factor-alpha; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC4087619
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55. Laskowitz DT, Song P, Wang H, Mace B, Sullivan PM, Vitek MP, Dawson HN: Traumatic brain injury exacerbates neurodegenerative pathology: improvement with an apolipoprotein E-based therapeutic. J Neurotrauma; 2010 Nov;27(11):1983-95
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  • We demonstrate that TBI accelerates neurodegenerative pathology in double-transgenic animals expressing the common human apoE alleles and mutated amyloid precursor protein, and that pathology is exacerbated in the presence of the apoE4 allele.
  • [MeSH-minor] Amyloid beta-Peptides / metabolism. Animals. Blotting, Western. Brain / pathology. Cytokines / biosynthesis. Enzyme-Linked Immunosorbent Assay. Gliosis / pathology. Humans. Immunohistochemistry. Male. Mice. Mice, Transgenic. Motor Activity / physiology. Platelet-Derived Growth Factor / genetics. Polymorphism, Genetic / genetics. Psychomotor Performance / physiology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Tumor Necrosis Factor-alpha / metabolism. tau Proteins / metabolism

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  • (PMID = 20812776.001).
  • [ISSN] 1557-9042
  • [Journal-full-title] Journal of neurotrauma
  • [ISO-abbreviation] J. Neurotrauma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Apolipoproteins E; 0 / Cytokines; 0 / Platelet-Derived Growth Factor; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 0 / tau Proteins
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56. Zhu X, Mei M, Lee HG, Wang Y, Han J, Perry G, Smith MA: P38 activation mediates amyloid-beta cytotoxicity. Neurochem Res; 2005 Jun-Jul;30(6-7):791-6
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  • [Title] P38 activation mediates amyloid-beta cytotoxicity.
  • Amyloid-beta is a leading candidate factor in the development of Alzheimer disease (AD), however the mechanisms involved are unclear.
  • As such, there has been considerable interest in evidence showing that the neuronal damage caused by amyloid-beta is mediated by oxidative stress.
  • One SAPK in particular, p38, appears to be crucial in AD and therefore, in the current study, we investigated the role of p38 activation in amyloid-beta cytotoxicity.
  • Our data showed p38 activation was induced by amyloid-beta in a concentration-dependent manner in M17 human neuroblastoma cells.
  • Notably, amyloid-beta toxicity was significantly decreased by inhibition of p38 activity by overexpressing dominant negative p38.
  • Consistent with this, in primary cortical neurons amyloid-beta also induced p38 activation and amyloid-beta toxicity was significantly diminished when p38 was inhibited by its specific inhibitor, SB203580.
  • Taken together, these data suggest that p38 is a key downstream effector of amyloid-beta-induced neuronal death and blocking this pathway may be of therapeutic value.
  • [MeSH-major] Amyloid beta-Peptides / physiology. p38 Mitogen-Activated Protein Kinases / metabolism
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Enzyme Activation. Humans. Neuroblastoma / enzymology. Neuroblastoma / metabolism. Neuroblastoma / pathology. Neurons / enzymology. Neurons / metabolism. Oxidative Stress

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  • (PMID = 16187214.001).
  • [ISSN] 0364-3190
  • [Journal-full-title] Neurochemical research
  • [ISO-abbreviation] Neurochem. Res.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / NS38648
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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57. Henriques AG, Vieira SI, Crespo-López ME, Guiomar de Oliveira MA, da Cruz e Silva EF, da Cruz e Silva OA: Intracellular sAPP retention in response to Abeta is mapped to cytoskeleton-associated structures. J Neurosci Res; 2009 May 1;87(6):1449-61
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  • Amyloid beta (Abeta) contributes to neurodegeneration in Alzheimer's disease and provides a close association between molecular events and pathology, although the underlying molecular mechanisms are unclear.
  • In the work described here, Abeta did not induce amyloid precursor protein (APP) expression, but APP processing/trafficking was markedly affected.
  • [MeSH-major] Amyloid beta-Peptides / metabolism. Amyloid beta-Protein Precursor / metabolism. Cytoskeleton / metabolism. Neurons / metabolism
  • [MeSH-minor] Analysis of Variance. Animals. Blotting, Northern. COS Cells. Cell Line. Cell Line, Tumor. Cercopithecus aethiops. Gene Expression. Immunohistochemistry. PC12 Cells. RNA / metabolism. Rats. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19105196.001).
  • [ISSN] 1097-4547
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Amyloid beta-Protein Precursor; 63231-63-0 / RNA
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58. Cenini G, Cecchi C, Pensalfini A, Bonini SA, Ferrari-Toninelli G, Liguri G, Memo M, Uberti D: Generation of reactive oxygen species by beta amyloid fibrils and oligomers involves different intra/extracellular pathways. Amino Acids; 2010 Apr;38(4):1101-6
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  • [Title] Generation of reactive oxygen species by beta amyloid fibrils and oligomers involves different intra/extracellular pathways.
  • A neuropathological characteristic of Alzheimer's disease is the extracellular accumulation of amyloid beta peptide (Abeta) in neuritic plaques.
  • [MeSH-major] Alzheimer Disease / physiopathology. Amyloid / metabolism. Amyloid beta-Peptides / metabolism. Peptide Fragments / metabolism. Reactive Oxygen Species / metabolism
  • [MeSH-minor] Adsorption / drug effects. Biological Transport / drug effects. Cell Line, Tumor. Cell Membrane / metabolism. Cell Survival / drug effects. Colchicine / pharmacology. Cytoskeleton / drug effects. Cytosol / metabolism. Endocytosis / drug effects. Humans. Intracellular Membranes / metabolism. Microscopy, Confocal. Neurons / drug effects. Neurons / pathology

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  • [ErratumIn] Amino Acids. 2010 Apr;38(4):1107. Giovanna, Cenini [corrected to Cenini, Giovanna]
  • (PMID = 19582548.001).
  • [ISSN] 1438-2199
  • [Journal-full-title] Amino acids
  • [ISO-abbreviation] Amino Acids
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Amyloid; 0 / Amyloid beta-Peptides; 0 / Peptide Fragments; 0 / Reactive Oxygen Species; 0 / amyloid beta-protein (1-42); SML2Y3J35T / Colchicine
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59. Cavallaro RA, Fuso A, D'Anselmi F, Seminara L, Scarpa S: The effect of S-adenosylmethionine on CNS gene expression studied by cDNA microarray analysis. J Alzheimers Dis; 2006 Aug;9(4):415-9
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  • It has already been shown that DNA methylation is involved in amyloid-beta-protein precursor (AbetaPP) processing and amyloid-beta(Abeta) production through the regulation of Presenilin 1 (PS1) expression and that exogenous SAM can silence the gene reducing Abeta.
  • [MeSH-minor] Aging. Amyloid beta-Protein Precursor / drug effects. Cell Line, Tumor / pathology. Chromatography, High Pressure Liquid. DNA Methylation / drug effects. Humans. Membrane Proteins / drug effects. Membrane Proteins / metabolism. Neuroblastoma / metabolism. Neuroblastoma / pathology. Presenilin-1. RNA / drug effects. RNA / genetics. RNA / metabolism

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  • (PMID = 16917150.001).
  • [ISSN] 1387-2877
  • [Journal-full-title] Journal of Alzheimer's disease : JAD
  • [ISO-abbreviation] J. Alzheimers Dis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Membrane Proteins; 0 / PSEN1 protein, human; 0 / Presenilin-1; 63231-63-0 / RNA; 7LP2MPO46S / S-Adenosylmethionine
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60. Zahradník FJ: Quantitative analysis of streptococcal exoprotein flow to the host receptor--exact basis for therapy of tumors and Alzheimer's disease. Folia Microbiol (Praha); 2005;50(1):63-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Alzheimer Disease / drug therapy. Alzheimer Disease / metabolism. Amyloid beta-Peptides / metabolism. Bacterial Proteins / metabolism. Biomarkers, Tumor / metabolism. Humans. Intracellular Signaling Peptides and Proteins / metabolism. Neoplasms / drug therapy. Neoplasms / metabolism. Peptides / metabolism. Protein Binding

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  • [ISSN] 0015-5632
  • [Journal-full-title] Folia microbiologica
  • [ISO-abbreviation] Folia Microbiol. (Praha)
  • [Language] eng
  • [Publication-type] Journal Article
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  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Bacterial Proteins; 0 / Biomarkers, Tumor; 0 / Intracellular Signaling Peptides and Proteins; 0 / Peptides; 0 / humanin; EC 3.2.2.5 / NAD+ Nucleosidase
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61. Di Segni A, Shaharabani E, Stein R, Pinkas-Kramarski R: Neuregulins rescue PC12-ErbB-4 cells from cell death induced by beta-amyloid peptide: involvement of PI3K and PKC. J Mol Neurosci; 2005;26(1):57-69
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  • [Title] Neuregulins rescue PC12-ErbB-4 cells from cell death induced by beta-amyloid peptide: involvement of PI3K and PKC.
  • We previously showed that NRG mediates survival of PC12-ErbB-4 cells from apoptosis induced by serum deprivation, tumor necrosis factor-alpha treatment, or H2O2.
  • In the present study, we show that NRG induces a significant protective effect from beta-amyloid 25-35 (Abeta[25-35]) peptide-induced cell death.
  • [MeSH-major] Amyloid beta-Protein Precursor / pharmacology. Cell Death / drug effects. Cell Survival / drug effects. Neuregulin-1 / pharmacology. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 15968086.001).
  • [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 / Amyloid beta-Protein Precursor; 0 / Neuregulin-1; 0 / Recombinant Proteins; 0 / neuregulin beta; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / ERBB4 protein, human; EC 2.7.10.1 / Erbb4 protein, rat; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-4; EC 2.7.11.13 / Protein Kinase C; NI40JAQ945 / Tetradecanoylphorbol Acetate
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62. Burns DM, Li YL, Shi E, He C, Xu M, Zhuo J, Zhang C, Qian DQ, Li Y, Wynn R, Covington MB, Katiyar K, Marando CA, Fridman JS, Scherle P, Friedman S, Metcalf B, Yao W: Compelling P1 substituent affect on metalloprotease binding profile enables the design of a novel cyclohexyl core scaffold with excellent MMP selectivity and HER-2 sheddase inhibition. Bioorg Med Chem Lett; 2009 Jul 1;19(13):3525-30
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] ADAM Proteins / metabolism. Amyloid Precursor Protein Secretases / metabolism. Antineoplastic Agents / chemical synthesis. Hydroxamic Acids / chemical synthesis. Membrane Proteins / metabolism. Receptor, ErbB-2 / metabolism
  • [MeSH-minor] Cell Line, Tumor. Drug Design. Humans. Matrix Metalloproteinase 2 / metabolism. Protein Binding. Structure-Activity Relationship. Substrate Specificity

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  • (PMID = 19457660.001).
  • [ISSN] 1464-3405
  • [Journal-full-title] Bioorganic & medicinal chemistry letters
  • [ISO-abbreviation] Bioorg. Med. Chem. Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydroxamic Acids; 0 / Membrane Proteins; EC 2.7.10.1 / Receptor, ErbB-2; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.81 / ADAM10 protein, human
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63. Zhang D, Hanson R, Roongta V, Dischino DD, Gao Q, Sloan CP, Polson C, Keavy D, Zheng M, Mitroka J, Yeola S: In vitro and in vivo metabolism of a gamma-secretase inhibitor BMS-299897 and generation of active metabolites in milligram quantities with a microbial bioreactor. Curr Drug Metab; 2006 Dec;7(8):883-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Butyrates / metabolism. Cunninghamella / metabolism. Enzyme Inhibitors / metabolism. Hydrocarbons, Halogenated / metabolism
  • [MeSH-minor] Animals. Bile / metabolism. Bioreactors. Biotransformation. Carbon Radioisotopes. Cell Line, Tumor. Cells, Cultured. Dogs. Drug Evaluation, Preclinical. Glucuronides / metabolism. Hepatocytes / metabolism. Humans. Macaca fascicularis. Male. Microsomes, Liver / metabolism. Rats. Rats, Sprague-Dawley

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  • (PMID = 17168689.001).
  • [ISSN] 1389-2002
  • [Journal-full-title] Current drug metabolism
  • [ISO-abbreviation] Curr. Drug Metab.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / 4-(2-((1R)-1-(((4-chlorophenyl)sulfonyl)-2,5-difluoroanilino)ethyl)-5-fluorophenyl)butanoic acid; 0 / Butyrates; 0 / Carbon Radioisotopes; 0 / Enzyme Inhibitors; 0 / Glucuronides; 0 / Hydrocarbons, Halogenated; EC 3.4.- / Amyloid Precursor Protein Secretases
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64. Qin B, Cartier L, Dubois-Dauphin M, Li B, Serrander L, Krause KH: A key role for the microglial NADPH oxidase in APP-dependent killing of neurons. Neurobiol Aging; 2006 Nov;27(11):1577-87
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  • Reactive oxygen species (ROS) and deposition of cleaved products of amyloid precursor protein (APP) are thought to contribute to neuronal loss observed in Alzheimer's disease (AD).

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  • (PMID = 16260066.001).
  • [ISSN] 1558-1497
  • [Journal-full-title] Neurobiology of aging
  • [ISO-abbreviation] Neurobiol. Aging
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01 AG019519; United States / NIAID NIH HHS / AI / R01 AI020866; United States / NIA NIH HHS / AG / AG19519-01; United States / NIAID NIH HHS / AI / AI20866-18
  • [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 / APP protein, human; 0 / Amyloid beta-Protein Precursor; 0 / Antioxidants; 0 / Enzyme Inhibitors; 0 / Onium Compounds; 0 / Protease Nexins; 0 / Reactive Oxygen Species; 0 / Receptors, Cell Surface; 1406-18-4 / Vitamin E; 6HJ411TU98 / diphenyleneiodonium; EC 1.6.3.1 / NADPH Oxidase; PQ6CK8PD0R / Ascorbic Acid
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65. Pinweha S, Wanikiat P, Sanvarinda Y, Supavilai P: The signaling cascades of Ganoderma lucidum extracts in stimulating non-amyloidogenic protein secretion in human neuroblastoma SH-SY5Y cell lines. Neurosci Lett; 2008 Dec 19;448(1):62-6
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  • In this study, we have investigated the effect of GL mycelia extracts on the non-amyloidogenic protein secretion (sAPPalpha) and the amyloid precursor protein (APP) expression in SH-SY5Y neuroblastoma cells.
  • [MeSH-major] Amyloid Precursor Protein Secretases / metabolism. Amyloid beta-Protein Precursor / metabolism. Complex Mixtures / pharmacology. Reishi / chemistry. Signal Transduction / drug effects
  • [MeSH-minor] Cell Line, Tumor. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Neuroblastoma / metabolism. Protein Kinase C / metabolism

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  • (PMID = 18938219.001).
  • [ISSN] 0304-3940
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Complex Mixtures; 0 / Enzyme Inhibitors; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.- / Amyloid Precursor Protein Secretases
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66. Moss ML, Bomar M, Liu Q, Sage H, Dempsey P, Lenhart PM, Gillispie PA, Stoeck A, Wildeboer D, Bartsch JW, Palmisano R, Zhou P: The ADAM10 prodomain is a specific inhibitor of ADAM10 proteolytic activity and inhibits cellular shedding events. J Biol Chem; 2007 Dec 7;282(49):35712-21
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  • ADAM10 is a disintegrin metalloproteinase that processes amyloid precursor protein and ErbB ligands and is involved in the shedding of many type I and type II single membrane-spanning proteins.
  • Like tumor necrosis factor-alpha-converting enzyme (TACE or ADAM17), ADAM10 is expressed as a zymogen, and removal of the prodomain results in its activation.
  • [MeSH-major] ADAM Proteins / antagonists & inhibitors. ADAM Proteins / metabolism. Amyloid Precursor Protein Secretases / antagonists & inhibitors. Amyloid Precursor Protein Secretases / metabolism. Enzyme Precursors / antagonists & inhibitors. Enzyme Precursors / metabolism. Intercellular Signaling Peptides and Proteins / metabolism. Membrane Proteins / antagonists & inhibitors. Membrane Proteins / metabolism
  • [MeSH-minor] Amyloid beta-Protein Precursor / metabolism. Animals. Antigens, CD / metabolism. Betacellulin. COS Cells. Cercopithecus aethiops. Disintegrins / antagonists & inhibitors. Disintegrins / metabolism. Disintegrins / therapeutic use. Humans. Mice. Neoplasms / drug therapy. Neoplasms / enzymology. Protein Structure, Tertiary / physiology. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 17895248.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK59778; United States / NIDDK NIH HHS / DK / DK63363
  • [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 / Amyloid beta-Protein Precursor; 0 / Antigens, CD; 0 / BTC protein, human; 0 / Betacellulin; 0 / Btc protein, mouse; 0 / Disintegrins; 0 / Enzyme Precursors; 0 / Intercellular Signaling Peptides and Proteins; 0 / Membrane Proteins; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / Adam8 protein, mouse; EC 3.4.24.- / tumor necrosis factor-alpha convertase; EC 3.4.24.81 / ADAM10 protein, human
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67. Taddei K, Laws SM, Verdile G, Munns S, D'Costa K, Harvey AR, Martins IJ, Hill F, Levy E, Shaw JE, Martins RN: Novel phage peptides attenuate beta amyloid-42 catalysed hydrogen peroxide production and associated neurotoxicity. Neurobiol Aging; 2010 Feb;31(2):203-14
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  • [Title] Novel phage peptides attenuate beta amyloid-42 catalysed hydrogen peroxide production and associated neurotoxicity.
  • Amyloid-beta (Abeta) peptides play a central role in the pathogenesis of Alzheimer's disease.
  • [MeSH-major] Amyloid beta-Peptides / metabolism. Bacteriophages / metabolism. Hydrogen Peroxide / metabolism. Neurons / physiology. Peptide Fragments / metabolism. Peptides / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / physiology. Clioquinol / pharmacology. Escherichia coli / virology. Genetic Techniques. Humans. Hydro-Lyases / metabolism. Neuroprotective Agents / pharmacology. Peptide Library. Protein Binding. Rats. Sequence Analysis, DNA. Superoxide Dismutase / metabolism

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  • (PMID = 18472186.001).
  • [ISSN] 1558-1497
  • [Journal-full-title] Neurobiology of aging
  • [ISO-abbreviation] Neurobiol. Aging
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Neuroprotective Agents; 0 / Peptide Fragments; 0 / Peptide Library; 0 / Peptides; 0 / amyloid beta-protein (1-40); 0 / amyloid beta-protein (1-42); 7BHQ856EJ5 / Clioquinol; BBX060AN9V / Hydrogen Peroxide; EC 1.15.1.1 / Superoxide Dismutase; EC 4.2.1.- / Hydro-Lyases; EC 4.2.1.54 / lactate dehydratase
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68. Visser K, Smith C, Louw A: Interplay of the inflammatory and stress systems in a hepatic cell line: interactions between glucocorticoid receptor agonists and interleukin-6. Endocrinology; 2010 Nov;151(11):5279-93
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  • Like Dex, both CpdA and IL-6 increase the positive APPs, serum amyloid A and C-reactive protein, and decrease the negative APP, corticosteroid binding globulin.
  • [MeSH-minor] Analysis of Variance. Animals. Blotting, Western. Cell Line, Tumor. Cells, Cultured. Dexamethasone / pharmacology. Enzyme-Linked Immunosorbent Assay. Glucocorticoids / pharmacology. Mice. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 20881254.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Interleukin-6; 0 / Receptors, Glucocorticoid; 7S5I7G3JQL / Dexamethasone
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69. Schwarz N, Pruessmeyer J, Hess FM, Dreymueller D, Pantaler E, Koelsch A, Windoffer R, Voss M, Sarabi A, Weber C, Sechi AS, Uhlig S, Ludwig A: Requirements for leukocyte transmigration via the transmembrane chemokine CX3CL1. Cell Mol Life Sci; 2010 Dec;67(24):4233-48
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  • [MeSH-minor] ADAM Proteins / genetics. ADAM Proteins / metabolism. ADAM10 Protein. ADAM17 Protein. Amino Acid Sequence. Amyloid Precursor Protein Secretases / genetics. Amyloid Precursor Protein Secretases / metabolism. Animals. Calcium Signaling / physiology. Cell Line, Tumor. Cells, Cultured. Chemotaxis / physiology. Endothelial Cells / cytology. Endothelial Cells / physiology. Epithelial Cells / cytology. Epithelial Cells / physiology. Humans. Ligands. Membrane Proteins / genetics. Membrane Proteins / metabolism. Molecular Sequence Data. Protein Structure, Secondary. Receptors, Chemokine / chemistry. Receptors, Chemokine / genetics. Receptors, Chemokine / metabolism

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  • (PMID = 20559678.001).
  • [ISSN] 1420-9071
  • [Journal-full-title] Cellular and molecular life sciences : CMLS
  • [ISO-abbreviation] Cell. Mol. Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / CX3CL1 protein, human; 0 / CX3CR1 protein, human; 0 / Chemokine CX3CL1; 0 / Ligands; 0 / Membrane Proteins; 0 / Receptors, Chemokine; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.81 / ADAM10 Protein; EC 3.4.24.81 / ADAM10 protein, human; EC 3.4.24.86 / ADAM17 Protein
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70. Yanagida K, Okochi M, Tagami S, Nakayama T, Kodama TS, Nishitomi K, Jiang J, Mori K, Tatsumi S, Arai T, Ikeuchi T, Kasuga K, Tokuda T, Kondo M, Ikeda M, Deguchi K, Kazui H, Tanaka T, Morihara T, Hashimoto R, Kudo T, Steiner H, Haass C, Tsuchiya K, Akiyama H, Kuwano R, Takeda M: The 28-amino acid form of an APLP1-derived Abeta-like peptide is a surrogate marker for Abeta42 production in the central nervous system. EMBO Mol Med; 2009 Jul;1(4):223-35
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  • Surrogate markers for the Alzheimer disease (AD)-associated 42-amino acid form of amyloid-beta (Abeta42) have been sought because they may aid in the diagnosis of AD and for clarification of disease pathogenesis.
  • [MeSH-major] Alzheimer Disease / diagnosis. Amyloid beta-Protein Precursor / cerebrospinal fluid. Biomarkers / cerebrospinal fluid. Peptide Fragments / cerebrospinal fluid
  • [MeSH-minor] Adult. Amino Acid Sequence. Amyloid Precursor Protein Secretases / antagonists & inhibitors. Amyloid Precursor Protein Secretases / metabolism. Aspartic Acid Endopeptidases / antagonists & inhibitors. Aspartic Acid Endopeptidases / metabolism. Cell Line. Cell Line, Tumor. Humans. Middle Aged. Molecular Sequence Data. Mutation. Presenilin-1 / genetics

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  • (PMID = 20049724.001).
  • [ISSN] 1757-4684
  • [Journal-full-title] EMBO molecular medicine
  • [ISO-abbreviation] EMBO Mol Med
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / APLP1 protein, human; 0 / Amyloid beta-Protein Precursor; 0 / Biomarkers; 0 / PSEN1 protein, human; 0 / Peptide Fragments; 0 / Presenilin-1; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human
  • [Other-IDs] NLM/ PMC3378133
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71. Tamura Y, Hamajima K, Matsui K, Yanoma S, Narita M, Tajima N, Xin KQ, Klinman D, Okuda K: The F(ab)'2 fragment of an Abeta-specific monoclonal antibody reduces Abeta deposits in the brain. Neurobiol Dis; 2005 Nov;20(2):541-9
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  • This work examines whether administering the F(ab' )2 fragment of an IgG1 monoclonal antibody (mAb) targeting the N-terminal 1-13 amino acids of the beta-amyloid peptide (Abeta mAb) reduces amyloid deposition in Alzheimer's disease (AD).
  • Since IgG1 Abs do not fix complement, these findings suggest that effective in vivo clearance of amyloid deposits can be achieved without stimulation of FcR-reactive phagocytes or activation of the complement cascade.
  • [MeSH-major] Alzheimer Disease / drug therapy. Amyloid beta-Peptides / antagonists & inhibitors. Antibodies, Monoclonal / pharmacology. Immunoglobulin Fab Fragments / pharmacology. Plaque, Amyloid / drug effects
  • [MeSH-minor] Animals. Brain / drug effects. Brain / immunology. Brain / physiopathology. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / physiology. Complement System Proteins / drug effects. Complement System Proteins / immunology. Complement System Proteins / metabolism. Disease Models, Animal. Encephalitis / drug therapy. Encephalitis / immunology. Encephalitis / prevention & control. Injections, Intraperitoneal. Injections, Intraventricular. Mice. Mice, Transgenic. Peptide Fragments / antagonists & inhibitors. Peptide Fragments / chemistry. Peptide Fragments / immunology. Phagocytes / drug effects. Phagocytes / physiology. Protein Structure, Tertiary / drug effects. Protein Structure, Tertiary / physiology

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  • (PMID = 15908227.001).
  • [ISSN] 0969-9961
  • [Journal-full-title] Neurobiology of disease
  • [ISO-abbreviation] Neurobiol. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Fab Fragments; 0 / Peptide Fragments; 0 / amyloid beta-protein (1-40); 0 / amyloid beta-protein (1-42); 9007-36-7 / Complement System Proteins
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72. Wasilewska-Sampaio AP, Silveira MS, Holub O, Goecking R, Gomes FC, Neto VM, Linden R, Ferreira ST, De Felice FG: Neuritogenesis and neuronal differentiation promoted by 2,4-dinitrophenol, a novel anti-amyloidogenic compound. FASEB J; 2005 Oct;19(12):1627-36
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  • We examined the effects of 2,4-dinitrophenol (DNP), a recently described blocker of the aggregation and neurotoxicity of the beta-amyloid peptide, on neurite elongation of central neurons.
  • [MeSH-major] 2,4-Dinitrophenol / pharmacology. Amyloid / chemistry. Neurites / pathology. Neurons / metabolism
  • [MeSH-minor] Amyloid beta-Peptides / chemistry. Animals. Blotting, Western. Cell Differentiation. Cell Line. Cell Line, Tumor. Cerebral Cortex / pathology. Cyclic AMP / metabolism. Dose-Response Relationship, Drug. Extracellular Signal-Regulated MAP Kinases / metabolism. Hippocampus / cytology. Hippocampus / embryology. MAP Kinase Signaling System. Mice. Microscopy, Fluorescence. Neurodegenerative Diseases / pathology. Oxygen / metabolism. Oxygen Consumption. Peptide Fragments / chemistry. Rats. Reactive Oxygen Species. Time Factors. Uncoupling Agents / pharmacology. tau Proteins / chemistry

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  • (PMID = 16195371.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid; 0 / Amyloid beta-Peptides; 0 / Peptide Fragments; 0 / Reactive Oxygen Species; 0 / Uncoupling Agents; 0 / tau Proteins; E0399OZS9N / Cyclic AMP; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; Q13SKS21MN / 2,4-Dinitrophenol; S88TT14065 / Oxygen
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73. Wang Q, Li H, Liu N, Chen XY, Wu ML, Zhang KL, Kong QY, Liu J: Correlative analyses of notch signaling with resveratrol-induced differentiation and apoptosis of human medulloblastoma cells. Neurosci Lett; 2008 Jun 20;438(2):168-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Active Transport, Cell Nucleus / drug effects. Active Transport, Cell Nucleus / physiology. Amyloid Precursor Protein Secretases / antagonists & inhibitors. Amyloid Precursor Protein Secretases / metabolism. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Antioxidants / pharmacology. Antioxidants / therapeutic use. Apoptosis / drug effects. Apoptosis / physiology. Basic Helix-Loop-Helix Transcription Factors / drug effects. Basic Helix-Loop-Helix Transcription Factors / metabolism. Cell Differentiation / drug effects. Cell Differentiation / physiology. Cell Line, Tumor. Cell Proliferation / drug effects. Cytoplasm / drug effects. Cytoplasm / metabolism. Enzyme Inhibitors / pharmacology. Homeodomain Proteins / drug effects. Homeodomain Proteins / metabolism. Humans. Receptor, Notch1 / drug effects. Receptor, Notch1 / metabolism. Receptor, Notch2 / drug effects. Receptor, Notch2 / metabolism. Up-Regulation / drug effects. Up-Regulation / physiology

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  • (PMID = 18456406.001).
  • [ISSN] 0304-3940
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antioxidants; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Enzyme Inhibitors; 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / NOTCH2 protein, human; 0 / Receptor, Notch1; 0 / Receptor, Notch2; 0 / Receptors, Notch; 0 / Stilbenes; 149348-15-2 / HES1 protein, human; EC 3.4.- / Amyloid Precursor Protein Secretases; Q369O8926L / resveratrol
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74. Li YB, Wang R, Wu HL, Li YH, Zhong LJ, Yu HM, Li XJ: Serum amyloid A mediates the inhibitory effect of Ganoderma lucidum polysaccharides on tumor cell adhesion to endothelial cells. Oncol Rep; 2008 Sep;20(3):549-56
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  • [Title] Serum amyloid A mediates the inhibitory effect of Ganoderma lucidum polysaccharides on tumor cell adhesion to endothelial cells.
  • The present study was designed to determine the anti-tumor efficacy of GlPS and the possible mechanism covering this effect.
  • Three significantly changed proteins were identified by ESI-Q-TOF-MS and database search indicated that they were haptoblobin, apolipoprotein A-II and serum amyloid A (SAA), respectively.
  • Collectively, these results suggest that GlPS inhibited the tumor growth and tumor cell adhesion to HUVECs via up-regulation of SAA protein expression.
  • [MeSH-major] Cell Adhesion / drug effects. Endothelium, Vascular / metabolism. Polysaccharides / therapeutic use. Prostatic Neoplasms / metabolism. Reishi / chemistry. Sarcoma 180 / drug therapy. Serum Amyloid A Protein / metabolism

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  • (PMID = 18695905.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Polysaccharides; 0 / RNA, Messenger; 0 / Serum Amyloid A Protein
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75. Velez D, Hinojar-Gutierrez A, Nam-Cha S, Acevedo-Barbera A: Laryngeal plasmacytoma presenting as amyloid tumour: a case report. Eur Arch Otorhinolaryngol; 2007 Aug;264(8):959-61
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  • [Title] Laryngeal plasmacytoma presenting as amyloid tumour: a case report.
  • Immunohistochemical studies showed that the tumour cells of the plasmacytoma were monoclonal (lambda-restricted).
  • The amyloid deposits were also shown to be reactive with lambda immunoglobulin light chain, suggesting the pathogenetic relationship between the plasmacytoma and amyloid deposition in the larynx.
  • The majority of the cases reported of amyloid deposition with plasmacytoma, the lesions were found in the nasopharynx, in contrast to our case in which the lesions were sited in the larynx and with the peculiarity of being multiples.
  • Moreover, amyloid and plasmacytoma were clearly delimitated and the amyloid tissue was more extensive than the tumour tissue.

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76. Serdar A, Basak D, Sercan G, Ali V: Solitary amyloid tumor of the tongue base. Int J Otolaryngol; 2009;2009:515068
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  • [Title] Solitary amyloid tumor of the tongue base.
  • The purpose of this article is to present a rare case of localized, solitary amyloid tumor of tongue base and emphasize some of the characteristic features of challenging clinical and histopathologic diagnosis.
  • In this paper, we focused on the clinical and pathological specifications of this rare tumor, so any unnecessary examinations or measures may be spared.
  • Negative staining of amyloid material with AAC and osseous metaplasia noted in the histopathologic examination may not be thought as definite criteria for localized amyloidosis, but a supporter of localized, solitary amyloid tumor diagnosis.

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  • (PMID = 20107570.001).
  • [ISSN] 1687-921X
  • [Journal-full-title] International journal of otolaryngology
  • [ISO-abbreviation] Int J Otolaryngol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2809435
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77. von Arnim CA, von Einem B, Weber P, Wagner M, Schwanzar D, Spoelgen R, Strauss WL, Schneckenburger H: Impact of cholesterol level upon APP and BACE proximity and APP cleavage. Biochem Biophys Res Commun; 2008 May 30;370(2):207-12
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  • Cleavage of APP by BACE is the first proteolytic step in the production of Amyloid beta (Abeta, which accumulates in senile plaques in Alzheimer's disease.
  • [MeSH-major] Amyloid Precursor Protein Secretases / metabolism. Amyloid beta-Protein Precursor / metabolism. Aspartic Acid Endopeptidases / metabolism. Cell Membrane / metabolism. Cholesterol / metabolism. Fluorescence Resonance Energy Transfer / methods. Microscopy, Fluorescence / methods. Receptors, Cell Surface / metabolism
  • [MeSH-minor] Cell Line, Tumor. Green Fluorescent Proteins / analysis. Green Fluorescent Proteins / genetics. Humans. Membrane Fluidity. Protease Nexins

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  • (PMID = 18374657.001).
  • [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 / APP protein, human; 0 / Amyloid beta-Protein Precursor; 0 / Protease Nexins; 0 / Receptors, Cell Surface; 147336-22-9 / Green Fluorescent Proteins; 97C5T2UQ7J / Cholesterol; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 3.4.23.- / Aspartic Acid Endopeptidases; EC 3.4.23.46 / BACE1 protein, human
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78. Muñoz-Ruiz P, Rubio L, García-Palomero E, Dorronsoro I, del Monte-Millán M, Valenzuela R, Usán P, de Austria C, Bartolini M, Andrisano V, Bidon-Chanal A, Orozco M, Luque FJ, Medina M, Martínez A: Design, synthesis, and biological evaluation of dual binding site acetylcholinesterase inhibitors: new disease-modifying agents for Alzheimer's disease. J Med Chem; 2005 Nov 17;48(23):7223-33
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  • New dual binding site acetylcholinesterase (AChE) inhibitors have been designed and synthesized as new potent drugs that may simultaneously alleviate cognitive deficits and behave as disease-modifying agents by inhibiting the beta-amyloid (A beta) peptide aggregation through binding to both catalytic and peripheral sites of the enzyme.
  • [MeSH-major] Acetylcholinesterase / chemistry. Alzheimer Disease / drug therapy. Amyloid beta-Peptides / antagonists & inhibitors. Cholinesterase Inhibitors / chemical synthesis. Nootropic Agents / chemical synthesis. Tacrine / analogs & derivatives. Tacrine / chemical synthesis
  • [MeSH-minor] Animals. Binding Sites. Butyrylcholinesterase / chemistry. Cattle. Cell Line, Tumor. Dimerization. Drug Design. Erythrocytes / enzymology. Fluorometry. Humans. Models, Molecular. Protein Binding. Structure-Activity Relationship

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  • (PMID = 16279781.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Cholinesterase Inhibitors; 0 / Nootropic Agents; 4VX7YNB537 / Tacrine; EC 3.1.1.- / Butyrylcholinesterase; EC 3.1.1.7 / Acetylcholinesterase
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79. Elzinga BM, Twomey C, Powell JC, Harte F, McCarthy JV: Interleukin-1 receptor type 1 is a substrate for gamma-secretase-dependent regulated intramembrane proteolysis. J Biol Chem; 2009 Jan 16;284(3):1394-409
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  • In this study, we report the characterization of a highly conserved tumor necrosis factor receptor-associated factor-6 (TRAF6) consensus-binding site within the hydrophilic loop domain of presenilin-1 (PS-1).
  • [MeSH-major] Amyloid Precursor Protein Secretases / metabolism. Interleukin-1 Receptor-Associated Kinases / metabolism. Presenilin-1 / metabolism. Receptors, Interleukin-1 Type I / metabolism. TNF Receptor-Associated Factor 6 / metabolism

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  • (PMID = 18996842.001).
  • [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 / Cytokines; 0 / IL1R1 protein, human; 0 / Presenilin-1; 0 / Protease Inhibitors; 0 / Receptors, Interleukin-1 Type I; 0 / TNF Receptor-Associated Factor 6; EC 2.7.11.1 / Interleukin-1 Receptor-Associated Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 3.4.- / Amyloid Precursor Protein Secretases
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80. Tang H, Fu Y, Cui Y, He Y, Zeng X, Ploplis VA, Castellino FJ, Luo Y: Fibrinogen has chaperone-like activity. Biochem Biophys Res Commun; 2009 Jan 16;378(3):662-7
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  • [Title] Fibrinogen has chaperone-like activity.
  • Partially or completely unfolded polypeptides are highly prone to aggregation due to nonspecific interactions between their exposed hydrophobic surfaces.
  • Extracellular proteins are continuously subjected to stresses conditions, but the existence of extracellular chaperones remains largely unexplored.
  • The results presented here demonstrate that one of the most abundant extracellular proteins, fibrinogen has chaperone-like activity.
  • Fibrinogen can specifically bind to nonnative form of citrate synthase and inhibit its thermal aggregation and inactivation in an ATP-independent manner.
  • Interestingly, fibrinogen maintains thermal-denatured luciferase in a refolding competent state allowing luciferase to be refolded in cooperation with rabbit reticulocyte lysate.
  • Fibrinogen also inhibits fibril formation of yeast prion protein Sup35 (NM).
  • Furthermore, fibrinogen rescues thermal-induced protein aggregation in the plasma of fibrinogen-deficient mice.
  • Our studies demonstrate the chaperone-like activity of fibrinogen, which not only provides new insights into the extracellular chaperone protein system, but also suggests potential diagnostic and therapeutic approaches to fibrinogen-related pathological conditions.

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  • (PMID = 19059206.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL073750-01A19002; United States / NHLBI NIH HHS / HL / P01 HL073750; United States / NHLBI NIH HHS / HL / HL073750; United States / NHLBI NIH HHS / HL / P01 HL073750-01A19002
  • [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 / Amyloid; 0 / Molecular Chaperones; 0 / Peptide Termination Factors; 0 / Prions; 0 / SUP35 protein, S cerevisiae; 0 / Saccharomyces cerevisiae Proteins; 9001-32-5 / Fibrinogen; EC 1.13.12.7 / Luciferases, Firefly; EC 2.3.3.1 / Citrate (si)-Synthase
  • [Other-IDs] NLM/ NIHMS92328; NLM/ PMC2663026
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81. Rustighi A, Tiberi L, Soldano A, Napoli M, Nuciforo P, Rosato A, Kaplan F, Capobianco A, Pece S, Di Fiore PP, Del Sal G: The prolyl-isomerase Pin1 is a Notch1 target that enhances Notch1 activation in cancer. Nat Cell Biol; 2009 Feb;11(2):133-42
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  • [MeSH-minor] Amyloid Precursor Protein Secretases / metabolism. Cell Line, Tumor. Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / metabolism. Enzyme Activation / genetics. Gene Expression Regulation, Neoplastic / genetics. Humans. Protein Structure, Tertiary / genetics. Transcriptional Activation / genetics

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  • (PMID = 19151708.001).
  • [ISSN] 1476-4679
  • [Journal-full-title] Nature cell biology
  • [ISO-abbreviation] Nat. Cell Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA-83736-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NIMA-interacting peptidylprolyl isomerase; 0 / NOTCH1 protein, human; 0 / Receptor, Notch1; EC 3.4.- / Amyloid Precursor Protein Secretases; EC 5.2.1.8 / Peptidylprolyl Isomerase
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82. Madeira A, Pommet JM, Prochiantz A, Allinquant B: SET protein (TAF1beta, I2PP2A) is involved in neuronal apoptosis induced by an amyloid precursor protein cytoplasmic subdomain. FASEB J; 2005 Nov;19(13):1905-7
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  • [Title] SET protein (TAF1beta, I2PP2A) is involved in neuronal apoptosis induced by an amyloid precursor protein cytoplasmic subdomain.
  • When overexpressed, a short cytoplasmic domain of the amyloid precursor protein (APP), normally unmasked in the brain of Alzheimer's disease patients, activates caspase-3 and induces neuronal death.
  • [MeSH-major] Amyloid beta-Protein Precursor / chemistry. Apoptosis. Chromosomal Proteins, Non-Histone / physiology. Cytoplasm / metabolism. Neurons / pathology. Transcription Factors / physiology
  • [MeSH-minor] Alzheimer Disease / metabolism. Animals. Aspartic Acid / chemistry. Biological Assay. Brain / embryology. Cell Death. Cell Line, Tumor. Cell Survival. Down-Regulation. Histone Chaperones. Humans. Immunohistochemistry. Mass Spectrometry. Models, Biological. Oligonucleotides, Antisense / chemistry. Oligonucleotides, Antisense / pharmacology. Peptides / chemistry. Protein Binding. Protein Structure, Tertiary. Rats. Recombinant Proteins / chemistry. Silver Staining. Tyrosine / chemistry

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  • (PMID = 16162853.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amyloid beta-Protein Precursor; 0 / Chromosomal Proteins, Non-Histone; 0 / Histone Chaperones; 0 / Oligonucleotides, Antisense; 0 / Peptides; 0 / Recombinant Proteins; 0 / SET protein, human; 0 / Transcription Factors; 30KYC7MIAI / Aspartic Acid; 42HK56048U / Tyrosine
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83. Rallidis LS, Hamodraka ES, Fountoulaki K, Moustogiannis G, Zolindaki MG, Kremastinos DT: Simvastatin exerts its anti-inflammatory effect in hypercholesterolaemic patients by decreasing the serum levels of monocyte chemoattractant protein-1. Int J Cardiol; 2008 Feb 29;124(2):271-2
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  • AIM: To assess the effect of simvastatin on serum levels of monocyte chemoattractant protein-1 (MCP-1), interleukin-6, tumor necrosis factor-alpha, macrophage colony stimulating factor, C-reactive protein and serum amyloid A in hypercholesterolaemic patients without coronary heart disease.
  • [MeSH-minor] Adult. Aged. Amyloid / blood. Amyloid / drug effects. Biomarkers / blood. C-Reactive Protein / drug effects. C-Reactive Protein / metabolism. Cardiovascular Diseases / prevention & control. Cytokines / drug effects. Cytokines / metabolism. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Male. Middle Aged. Probability. Reference Values. Risk Factors. Sensitivity and Specificity. Severity of Illness Index. Treatment Outcome

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  • (PMID = 17399814.001).
  • [ISSN] 1874-1754
  • [Journal-full-title] International journal of cardiology
  • [ISO-abbreviation] Int. J. Cardiol.
  • [Language] eng
  • [Publication-type] Letter; Randomized Controlled Trial
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Amyloid; 0 / Biomarkers; 0 / Chemokine CCL2; 0 / Cytokines; 9007-41-4 / C-Reactive Protein; AGG2FN16EV / Simvastatin
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84. Wang R, Chadalavada K, Wilshire J, Kowalik U, Hovinga KE, Geber A, Fligelman B, Leversha M, Brennan C, Tabar V: Glioblastoma stem-like cells give rise to tumour endothelium. Nature; 2010 Dec 09;468(7325):829-33
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  • [Title] Glioblastoma stem-like cells give rise to tumour endothelium.
  • Yet the mechanisms of angiogenesis and the origin of tumour endothelial cells remain poorly defined.
  • Here we demonstrate that a subpopulation of endothelial cells within glioblastomas harbour the same somatic mutations identified within tumour cells, such as amplification of EGFR and chromosome 7.
  • Extensive in vitro and in vivo lineage analyses, including single cell clonal studies, further show that a subpopulation of the CD133(+) stem-like cell fraction is multipotent and capable of differentiation along tumour and endothelial lineages, possibly via an intermediate CD133(+)/CD144(+) progenitor cell.
  • The findings are supported by genetic studies of specific exons selected from The Cancer Genome Atlas, quantitative FISH and comparative genomic hybridization data that demonstrate identical genomic profiles in the CD133(+) tumour cells, their endothelial progenitor derivatives and mature endothelium.
  • Exposure to the clinical anti-angiogenesis agent bevacizumab or to a γ-secretase inhibitor as well as knockdown shRNA studies demonstrate that blocking VEGF or silencing VEGFR2 inhibits the maturation of tumour endothelial progenitors into endothelium but not the differentiation of CD133(+) cells into endothelial progenitors, whereas γ-secretase inhibition or NOTCH1 silencing blocks the transition into endothelial progenitors.
  • The lineage plasticity and capacity to generate tumour vasculature of the putative cancer stem cells within glioblastoma are novel findings that provide new insight into the biology of gliomas and the definition of cancer stemness, as well as the mechanisms of tumour neo-angiogenesis.
  • [MeSH-minor] AC133 Antigen. Amyloid Precursor Protein Secretases / antagonists & inhibitors. Animals. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Antigens, CD / metabolism. Bevacizumab. Cadherins / deficiency. Cadherins / metabolism. Cell Line, Tumor. Cell Lineage. Chromosome Aberrations. Coculture Techniques. Female. Glycoproteins / metabolism. Humans. In Situ Hybridization, Fluorescence. Integrin beta4 / metabolism. Male. Mice. Mice, Inbred NOD. Mice, SCID. Peptides / metabolism. Receptor, Notch1 / deficiency. Receptor, Notch1 / genetics. Vascular Endothelial Growth Factor A / antagonists & inhibitors

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  • [CommentIn] Nat Rev Cancer. 2011 Jan;11(1):4 [21218530.001]
  • [CommentIn] Nat Rev Neurosci. 2011 Jan;12(1):3 [21218567.001]
  • [CommentIn] Nature. 2010 Dec 9;468(7325):770-1 [21150987.001]
  • (PMID = 21102433.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE24244/ GSE24446/ GSE24452/ GSE24557/ GSE24558
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AC133 Antigen; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Cadherins; 0 / Glycoproteins; 0 / Integrin beta4; 0 / PROM1 protein, human; 0 / Peptides; 0 / Prom1 protein, mouse; 0 / Receptor, Notch1; 0 / Vascular Endothelial Growth Factor A; 0 / cadherin 5; 2S9ZZM9Q9V / Bevacizumab; EC 3.4.- / Amyloid Precursor Protein Secretases
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85. Rasul S, Balasubramanian R, Filipović A, Slade MJ, Yagüe E, Coombes RC: Inhibition of gamma-secretase induces G2/M arrest and triggers apoptosis in breast cancer cells. Br J Cancer; 2009 Jun 16;100(12):1879-88
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  • [Title] Inhibition of gamma-secretase induces G2/M arrest and triggers apoptosis in breast cancer cells.
  • Gamma-secretase activity is vital for the transmembrane cleavage of Notch receptors and the subsequent migration of their intracellular domains to the nucleus.
  • Notch overexpression has been associated with breast, colon, cervical and prostate cancers.
  • We tested the effect of three different gamma-secretase inhibitors (GSIs) in breast cancer cells.
  • One inhibitor (GSI1) was lethal to breast cancer cell lines at concentrations of 2 muM and above but had a minimal effect on the non-malignant breast lines.
  • GSI1 was also cytotoxic for a wide variety of cancer cell lines in the NCI60 cell screen.
  • GSI1 treatment resulted in a marked decrease in gamma-secretase activity and downregulation of the Notch signalling pathway with no effects on expression of the gamma-secretase components or ligands.
  • Flow cytometric and western blot analyses indicated that GSI1 induces a G2/M arrest leading to apoptosis, through downregulation of Bcl-2, Bax and Bcl-XL.
  • GSI1 also inhibited proteasome activity.
  • Thus, the gamma-secretase inhibitor GSI1 has a complex mode of action to inhibit breast cancer cell survival and may represent a novel therapy in breast cancer.