Oxidative stress increases BACE1 protein levels through activation of the PKR-eIF2α pathway.
暂无分享,去创建一个
C. Bouras | J. Hugon | L. Pradier | F. Gray | C. Paquet | J. Dumurgier | F. Mouton-Liger
[1] C. Bouras,et al. The PKR Activator PACT Is Induced by Aβ: Involvement in Alzheimer's Disease , 2012, Brain pathology.
[2] J. Clarimón,et al. Activation of PKR Causes Amyloid ß-Peptide Accumulation via De-Repression of BACE1 Expression , 2011, PloS one.
[3] Jing Jing Li,et al. Differential regulation of BACE1 expression by oxidative and nitrosative signals , 2011, Molecular Neurodegeneration.
[4] J. Hugon,et al. Modulation of Tau Phosphorylation by the Kinase PKR: Implications in Alzheimer's Disease , 2011, Brain pathology.
[5] J. Hellemans,et al. BACE1 mRNA expression in Alzheimer's disease postmortem brain tissue. , 2011, Journal of Alzheimer's disease : JAD.
[6] J. Hugon,et al. Biogenesis and regulation of microRNA: implication in Alzheimer’s disease , 2010 .
[7] M. Ohno,et al. Phospho-eIF2α Level Is Important for Determining Abilities of BACE1 Reduction to Rescue Cholinergic Neurodegeneration and Memory Defects in 5XFAD Mice , 2010, PloS one.
[8] Zhenguo Wu,et al. Tyk2/STAT3 Signaling Mediates β-Amyloid-Induced Neuronal Cell Death: Implications in Alzheimer's Disease , 2010, The Journal of Neuroscience.
[9] M. Mattson,et al. An Overview of APP Processing Enzymes and Products , 2010, NeuroMolecular Medicine.
[10] C. Arias,et al. Oxidative stress promotes JNK-dependent amyloidogenic processing of normally expressed human APP by differential modification of α-, β- and γ-secretase expression , 2009, Neurochemistry International.
[11] H. Soininen,et al. Down-regulation of Seladin-1 Increases BACE1 Levels and Activity through Enhanced GGA3 Depletion during Apoptosis* , 2009, The Journal of Biological Chemistry.
[12] R. Chang,et al. Could PKR inhibition modulate human neurodegeneration? , 2009, Expert review of neurotherapeutics.
[13] Marie-Claude Potier,et al. Classification and basic pathology of Alzheimer disease , 2009, Acta Neuropathologica.
[14] D. Bennett,et al. Phosphorylation of the Translation Initiation Factor eIF2α Increases BACE1 Levels and Promotes Amyloidogenesis , 2008, Neuron.
[15] Shin-Hee Lee,et al. Oxidative stress induces PKR-dependent apoptosis via IFN-gamma activation signaling in Jurkat T cells. , 2008, Biochemical and biophysical research communications.
[16] R. Braun,et al. TRBP Control of PACT-Induced Phosphorylation of Protein Kinase R Is Reversed by Stress , 2008, Molecular and Cellular Biology.
[17] A. Delacourte,et al. Loss of microRNA cluster miR-29a/b-1 in sporadic Alzheimer's disease correlates with increased BACE1/β-secretase expression , 2008, Proceedings of the National Academy of Sciences.
[18] Bryan Maloney,et al. Transcriptional Regulation of β-Secretase by p25/cdk5 Leads to Enhanced Amyloidogenic Processing , 2008, Neuron.
[19] H. Cai,et al. Activation of protein kinase C modulates BACE1-mediated β-secretase activity , 2008, Neurobiology of Aging.
[20] Jia Luo,et al. Activation of double‐stranded RNA‐activated protein kinase by mild impairment of oxidative metabolism in neurons , 2007, Journal of neurochemistry.
[21] M. Mattson,et al. Oxidative stress activates a positive feedback between the γ‐ and β‐secretase cleavages of the β‐amyloid precursor protein , 2007 .
[22] S. Ingrand,et al. The oxindole/imidazole derivative C16 reduces in vivo brain PKR activation , 2007, FEBS letters.
[23] M. Tabaton,et al. The increased activity of BACE1 correlates with oxidative stress in Alzheimer's disease , 2007, Neurobiology of Aging.
[24] R. Tanzi,et al. Depletion of GGA3 Stabilizes BACE and Enhances β-Secretase Activity , 2007, Neuron.
[25] E. Meurs,et al. The dsRNA protein kinase PKR: virus and cell control. , 2007, Biochimie.
[26] M. Hentze,et al. Complex translational regulation of BACE1 involves upstream AUGs and stimulatory elements within the 5′ untranslated region , 2007, Nucleic acids research.
[27] R. Berry,et al. β-Site Amyloid Precursor Protein Cleaving Enzyme 1 Levels Become Elevated in Neurons around Amyloid Plaques: Implications for Alzheimer's Disease Pathogenesis , 2007, The Journal of Neuroscience.
[28] T. Bayer,et al. Activated double-stranded RNA-dependent protein kinase and neuronal death in models of Alzheimer’s disease , 2006, Neuroscience.
[29] C. Samuel,et al. Activation of the RNA-dependent Protein Kinase PKR Promoter in the Absence of Interferon Is Dependent Upon Sp Proteins* , 2006, Journal of Biological Chemistry.
[30] V. Kim,et al. The role of PACT in the RNA silencing pathway , 2006, The EMBO journal.
[31] Y. Li,et al. The FASEB Journal • Research Communication Control of APP processing and A � generation level by , 2022 .
[32] Randal J. Kaufman,et al. Divergent Roles of IRE1α and PERK in the Unfolded Protein Response , 2006 .
[33] P. Reddy. Amyloid precursor protein‐mediated free radicals and oxidative damage: Implications for the development and progression of Alzheimer's disease , 2006, Journal of neurochemistry.
[34] G. Pavitt,et al. eIF2B, a mediator of general and gene-specific translational control. , 2005, Biochemical Society transactions.
[35] L. Platanias. Mechanisms of type-I- and type-II-interferon-mediated signalling , 2005, Nature Reviews Immunology.
[36] C. Proud. eIF2 and the control of cell physiology. , 2005, Seminars in cell & developmental biology.
[37] J. Trojanowski,et al. BACE overexpression alters the subcellular processing of APP and inhibits Aβ deposition in vivo , 2005, The Journal of cell biology.
[38] D. Ron,et al. Translation reinitiation at alternative open reading frames regulates gene expression in an integrated stress response , 2004, The Journal of cell biology.
[39] T. Bayer,et al. Massive CA1/2 neuronal loss with intraneuronal and N-terminal truncated Abeta42 accumulation in a novel Alzheimer transgenic model. , 2004, The American journal of pathology.
[40] R. Wek,et al. Reinitiation involving upstream ORFs regulates ATF4 mRNA translation in mammalian cells. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[41] C. Haass,et al. Expression of the Alzheimer protease BACE1 is suppressed via its 5'‐untranslated region , 2004, EMBO reports.
[42] T. Südhof,et al. Cleavage of Amyloid-β Precursor Protein and Amyloid-β Precursor-like Protein by BACE 1* , 2004, Journal of Biological Chemistry.
[43] Marija Mihailovich,et al. Translational regulation of BACE-1 expression in neuronal and non-neuronal cells. , 2004, Nucleic acids research.
[44] Hong Qing,et al. Transcriptional Regulation of BACE1, the β-Amyloid Precursor Protein β-Secretase, by Sp1 , 2004, Molecular and Cellular Biology.
[45] D. Bredesen,et al. Activation of the cell stress kinase PKR in Alzheimer’s disease and human amyloid precursor protein transgenic mice , 2003, Neurobiology of Disease.
[46] N. Cairns,et al. Beta-secretase (BACE) and GSK-3 mRNA levels in Alzheimer's disease. , 2003, Brain research. Molecular brain research.
[47] J. Pestka,et al. Role of double-stranded RNA-activated protein kinase R (PKR) in deoxynivalenol-induced ribotoxic stress response. , 2003, Toxicological sciences : an official journal of the Society of Toxicology.
[48] R. Chang,et al. Phosphorylation of eukaryotic initiation factor-2&agr; (eIF2&agr;) is associated with neuronal degeneration in Alzheimer's disease , 2002, Neuroreport.
[49] Xiongwei Zhu,et al. Comparative biology and pathology of oxidative stress in Alzheimer and other neurodegenerative diseases: beyond damage and response. , 2002, Comparative biochemistry and physiology. Toxicology & pharmacology : CBP.
[50] R. Chang,et al. Involvement of double‐stranded RNA‐dependent protein kinase and phosphorylation of eukaryotic initiation factor‐2α in neuronal degeneration , 2002, Journal of neurochemistry.
[51] J. Pelletier,et al. An upstream open reading frame impedes translation of the huntingtin gene. , 2002, Nucleic acids research.
[52] B. Hyman,et al. Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease. , 2002, Archives of neurology.
[53] J. Hardy,et al. The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics , 2009 .
[54] J. Trojanowski,et al. The relationship between oxidative/nitrative stress and pathological inclusions in Alzheimer's and Parkinson's diseases. , 2002, Free radical biology & medicine.
[55] C. Masters,et al. Increased expression of the amyloid precursor β‐secretase in Alzheimer's disease , 2002 .
[56] T. E. Dever,et al. Gene-Specific Regulation by General Translation Factors , 2002, Cell.
[57] J. Trill,et al. Characterization of the Glycosylation Profiles of Alzheimer's β-Secretase Protein Asp-2 Expressed in a Variety of Cell Lines* , 2001, The Journal of Biological Chemistry.
[58] M. Pfaffl,et al. A new mathematical model for relative quantification in real-time RT-PCR. , 2001, Nucleic acids research.
[59] W. Richards,et al. Mice deficient in BACE1, the Alzheimer's β-secretase, have normal phenotype and abolished β-amyloid generation , 2001, Nature Neuroscience.
[60] D. Teplow,et al. A Furin-like Convertase Mediates Propeptide Cleavage of BACE, the Alzheimer's β-Secretase* , 2000, The Journal of Biological Chemistry.
[61] Rekha C. Patel,et al. PACT, a Stress-modulated Cellular Activator of Interferon-induced Double-stranded RNA-activated Protein Kinase, PKR* , 2000, The Journal of Biological Chemistry.
[62] B. Williams,et al. The protein kinase PKR is required for p38 MAPK activation and the innate immune response to bacterial endotoxin , 2000, The EMBO journal.
[63] Robert H. Silverman,et al. Activation of p38 Mitogen-Activated Protein Kinase and c-Jun NH2-Terminal Kinase by Double-Stranded RNA and Encephalomyocarditis Virus: Involvement of RNase L, Protein Kinase R, and Alternative Pathways , 2000, Molecular and Cellular Biology.
[64] J. Treanor,et al. Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE. , 1999, Science.
[65] Mingli Yang,et al. RAX, a Cellular Activator for Double-stranded RNA-dependent Protein Kinase during Stress Signaling* , 1999, The Journal of Biological Chemistry.
[66] D. Ron,et al. Protein translation and folding are coupled by an endoplasmic-reticulum-resident kinase , 1999, Nature.
[67] S. Der,et al. A double-stranded RNA-activated protein kinase-dependent pathway mediating stress-induced apoptosis. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[68] A. Hinnebusch. The eIF-2α kinases: regulators of protein synthesis in starvation and stress , 1994 .
[69] A. Koromilas,et al. Doxorubicin bypasses the cytoprotective effects of eIF2α phosphorylation and promotes PKR-mediated cell death , 2011, Cell Death and Differentiation.
[70] W. Markesbery,et al. Neuron specific toxicity of oligomeric amyloid-β: role for JUN-kinase and oxidative stress. , 2010, Journal of Alzheimer's disease : JAD.
[71] M. Mattson,et al. Oxidative stress activates a positive feedback between the gamma- and beta-secretase cleavages of the beta-amyloid precursor protein. , 2008, Journal of neurochemistry.
[72] H. Cai,et al. Activation of protein kinase C modulates BACE1-mediated beta-secretase activity. , 2008, Neurobiology of aging.
[73] R. Berry,et al. Beta-site amyloid precursor protein cleaving enzyme 1 levels become elevated in neurons around amyloid plaques: implications for Alzheimer's disease pathogenesis. , 2007, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[74] R. Tanzi,et al. Depletion of GGA3 stabilizes BACE and enhances beta-secretase activity. , 2007, Neuron.
[75] R. Kaufman,et al. Divergent roles of IRE1alpha and PERK in the unfolded protein response. , 2006, Current molecular medicine.
[76] Kai Long,et al. A selective inhibitor of eIF2alpha dephosphorylation protects cells from ER stress. , 2005, Science.
[77] T. Südhof,et al. Cleavage of amyloid-beta precursor protein and amyloid-beta precursor-like protein by BACE 1. , 2004, The Journal of biological chemistry.
[78] P. Wong,et al. Elevated β-secretase expression and enzymatic activity detected in sporadic Alzheimer disease , 2003, Nature Medicine.
[79] R. Chang,et al. Phosphorylation of eukaryotic initiation factor-2alpha (eIF2alpha) is associated with neuronal degeneration in Alzheimer's disease. , 2002, Neuroreport.
[80] C. Masters,et al. Increased expression of the amyloid precursor beta-secretase in Alzheimer's disease. , 2002, Annals of neurology.
[81] C. Proud,et al. Regulation of eukaryotic initiation factor eIF2B. , 2001, Progress in molecular and subcellular biology.
[82] H. Cai,et al. BACE1 is the major beta-secretase for generation of Abeta peptides by neurons. , 2001, Nature neuroscience.
[83] M. Clemens. Initiation factor eIF2 alpha phosphorylation in stress responses and apoptosis. , 2001, Progress in molecular and subcellular biology.
[84] W. Richards,et al. Mice deficient in BACE1, the Alzheimer's beta-secretase, have normal phenotype and abolished beta-amyloid generation. , 2001, Nature neuroscience.
[85] M. Clemens. Initiation Factor eIF2α Phosphorylation in Stress Responses and Apoptosis , 2001 .
[86] A. Hinnebusch. The eIF-2 alpha kinases: regulators of protein synthesis in starvation and stress. , 1994, Seminars in cell biology.