Oxidative stress increases BACE1 protein levels through activation of the PKR-eIF2α pathway.

[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.