Phosphorylation of the Translation Initiation Factor eIF2α Increases BACE1 Levels and Promotes Amyloidogenesis

[1]  R. Vassar,et al.  Linking vascular disorders and Alzheimer's disease: Potential involvement of BACE1 , 2009, Neurobiology of Aging.

[2]  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.

[3]  Bryan Maloney,et al.  Transcriptional Regulation of β-Secretase by p25/cdk5 Leads to Enhanced Amyloidogenic Processing , 2008, Neuron.

[4]  Guiliang Tang,et al.  The Expression of MicroRNA miR-107 Decreases Early in Alzheimer's Disease and May Accelerate Disease Progression through Regulation of β-Site Amyloid Precursor Protein-Cleaving Enzyme 1 , 2008, The Journal of Neuroscience.

[5]  R. Kaufman,et al.  The endoplasmic reticulum and the unfolded protein response. , 2007, Seminars in cell & developmental biology.

[6]  G. Fiskum,et al.  Mechanisms of impaired mitochondrial energy metabolism in acute and chronic neurodegenerative disorders , 2007, Journal of neuroscience research.

[7]  R. Tanzi,et al.  Depletion of GGA3 Stabilizes BACE and Enhances β-Secretase Activity , 2007, Neuron.

[8]  M. Hentze,et al.  Complex translational regulation of BACE1 involves upstream AUGs and stimulatory elements within the 5′ untranslated region , 2007, Nucleic acids research.

[9]  K. Nader,et al.  eIF2α Phosphorylation Bidirectionally Regulates the Switch from Short- to Long-Term Synaptic Plasticity and Memory , 2007, Cell.

[10]  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.

[11]  S. Santi,et al.  Early detection of Alzheimer’s disease using neuroimaging , 2007, Experimental Gerontology.

[12]  K. Blennow,et al.  Imaging and CSF Studies in the Preclinical Diagnosis of Alzheimer's Disease , 2007, Annals of the New York Academy of Sciences.

[13]  B. Lamb,et al.  Spatial and temporal control of age-related APP processing in genomic-based β-secretase transgenic mice , 2007, Neurobiology of Aging.

[14]  P. Saftig,et al.  Control of Peripheral Nerve Myelination by the ß-Secretase BACE1 , 2006, Science.

[15]  L. Tsai,et al.  p25/Cyclin-Dependent Kinase 5 Induces Production and Intraneuronal Accumulation of Amyloid β In Vivo , 2006, The Journal of Neuroscience.

[16]  M. Ohno,et al.  Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation , 2006, The Journal of Neuroscience.

[17]  E. Yilmaz,et al.  Chemical Chaperones Reduce ER Stress and Restore Glucose Homeostasis in a Mouse Model of Type 2 Diabetes , 2006, Science.

[18]  B. A. Castilho,et al.  Phosphorylation of the alpha subunit of translation initiation factor-2 by PKR mediates protein synthesis inhibition in the mouse brain during status epilepticus. , 2006, The Biochemical journal.

[19]  P. Polak,et al.  Cytoskeletal and cell contact control of the glucocorticoid pathway , 2006, Molecular and Cellular Endocrinology.

[20]  Acknowledgments , 2006, Molecular and Cellular Endocrinology.

[21]  Weihui Zhou,et al.  Leaky Scanning and Reinitiation Regulate BACE1 Gene Expression , 2006, Alzheimer's & Dementia.

[22]  L. Ozmen,et al.  BACE/APPV717F Double-Transgenic Mice Develop Cerebral Amyloidosis and Inflammation , 2006, Neurodegenerative Diseases.

[23]  D. Steinberg,et al.  The cytoskeletal network controls c-Jun translation in a UTR-dependent manner , 2006, Oncogene.

[24]  Randal J. Kaufman,et al.  Divergent Roles of IRE1α and PERK in the Unfolded Protein Response , 2006 .

[25]  M. Ohno,et al.  Temporal memory deficits in Alzheimer's mouse models: rescue by genetic deletion of BACE1 , 2006, The European journal of neuroscience.

[26]  H. Cai,et al.  BACE1, a Major Determinant of Selective Vulnerability of the Brain to Amyloid-β Amyloidogenesis, is Essential for Cognitive, Emotional, and Synaptic Functions , 2005, The Journal of Neuroscience.

[27]  W. Paschen,et al.  Cellular abnormalities linked to endoplasmic reticulum dysfunction in cerebrovascular disease--therapeutic potential. , 2005, Pharmacology & therapeutics.

[28]  R. Vassar,et al.  Energy inhibition elevates beta-secretase levels and activity and is potentially amyloidogenic in APP transgenic mice: possible early events in Alzheimer's disease pathogenesis. , 2005, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[29]  G. Pavitt,et al.  eIF2B, a mediator of general and gene-specific translational control. , 2005, Biochemical Society transactions.

[30]  B. Hyman,et al.  BACE Is Degraded via the Lysosomal Pathway* , 2005, Journal of Biological Chemistry.

[31]  Inder M Verma,et al.  Targeting BACE1 with siRNAs ameliorates Alzheimer disease neuropathology in a transgenic model , 2005, Nature Neuroscience.

[32]  K. Nader,et al.  Translational control of hippocampal synaptic plasticity and memory by the eIF2α kinase GCN2 , 2005, Nature.

[33]  P. Falkai,et al.  Traumatic brain injury: cause or risk of Alzheimer’s disease? A review of experimental studies , 2005, Journal of Neural Transmission.

[34]  H. Braak,et al.  Cognitive status correlates with neuropathologic stage in Parkinson disease , 2005, Neurology.

[35]  N. Sonenberg,et al.  Translational control in stress and apoptosis , 2005, Nature Reviews Molecular Cell Biology.

[36]  G. Perry,et al.  β‐Site APP cleaving enzyme up‐regulation induced by 4‐hydroxynonenal is mediated by stress‐activated protein kinases pathways , 2005, Journal of neurochemistry.

[37]  K. Plaschke,et al.  Amyloid precursor protein (APP) and its derivatives change after cellular energy depletion. An in vitro-study , 2005, Journal of Neural Transmission.

[38]  J. Trojanowski,et al.  BACE overexpression alters the subcellular processing of APP and inhibits Aβ deposition in vivo , 2005, The Journal of cell biology.

[39]  S. Younkin,et al.  Altered Amyloid-β Metabolism and Deposition in Genomic-based β-Secretase Transgenic Mice* , 2004, Journal of Biological Chemistry.

[40]  Azeem Majeed,et al.  The Epidemiology of the Comorbidity of Epilepsy in the General Population , 2004, Epilepsia.

[41]  C. DeCarli Vascular factors in dementia: an overview , 2004, Journal of the Neurological Sciences.

[42]  H. Qing,et al.  Degradation of BACE by the ubiquitin‐proteasome pathway , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[43]  Eric Klann,et al.  Synaptic plasticity and translation initiation. , 2004, Learning & memory.

[44]  C. Haass,et al.  Expression of the Alzheimer protease BACE1 is suppressed via its 5'‐untranslated region , 2004, EMBO reports.

[45]  Bryan Maloney,et al.  Gene structure and organization of the human β‐secretase (BACE) promoter , 2004 .

[46]  J. Simpkins,et al.  Increased β-secretase activity and expression in rats following transient cerebral ischemia , 2004, Brain Research.

[47]  S. Hoyer Glucose metabolism and insulin receptor signal transduction in Alzheimer disease. , 2004, European journal of pharmacology.

[48]  J. Sharp,et al.  Phosphorylation of eIF2alpha is involved in the signaling of indispensable amino acid deficiency in the anterior piriform cortex of the brain in rats. , 2004, The Journal of nutrition.

[49]  G. Edelman,et al.  Differential utilization of upstream AUGs in the beta-secretase mRNA suggests that a shunting mechanism regulates translation. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[50]  Marija Mihailovich,et al.  Translational regulation of BACE-1 expression in neuronal and non-neuronal cells. , 2004, Nucleic acids research.

[51]  J. Schneider,et al.  Neurofibrillary tangles mediate the association of amyloid load with clinical Alzheimer disease and level of cognitive function. , 2004, Archives of neurology.

[52]  Suzanne Craft,et al.  Insulin and neurodegenerative disease: shared and specific mechanisms , 2004, The Lancet Neurology.

[53]  R. Nitsch,et al.  Transgenic BACE expression in mouse neurons accelerates amyloid plaque pathology , 2004, Journal of Neural Transmission.

[54]  G. Ransmayr,et al.  Experimental traumatic brain injury in rats stimulates the expression, production and activity of Alzheimer’s disease β-secretase (BACE-1) , 2004, Journal of Neural Transmission.

[55]  M. Ohno,et al.  BACE1 Deficiency Rescues Memory Deficits and Cholinergic Dysfunction in a Mouse Model of Alzheimer's Disease , 2004, Neuron.

[56]  J. Fastbom,et al.  β‐secretase‐cleaved amyloid precursor protein in Alzheimer brain: a morphologic study , 2004, Journal of cellular and molecular medicine.

[57]  G. Alexander,et al.  Functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer's dementia , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[58]  D. Ron,et al.  Inhibition of a constitutive translation initiation factor 2α phosphatase, CReP, promotes survival of stressed cells , 2003, The Journal of cell biology.

[59]  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.

[60]  Wickliffe C Abraham,et al.  Roles of amyloid precursor protein and its fragments in regulating neural activity, plasticity and memory , 2003, Progress in Neurobiology.

[61]  B. Strooper,et al.  Aph-1, Pen-2, and Nicastrin with Presenilin Generate an Active γ-Secretase Complex , 2003, Neuron.

[62]  R. Malinow,et al.  APP Processing and Synaptic Function , 2003, Neuron.

[63]  Vesna Jelic,et al.  A critical discussion of the role of neuroimaging in mild cognitive impairment * , 2003, Acta neurologica Scandinavica. Supplementum.

[64]  G. Wilcock,et al.  alpha- and beta-secretase: profound changes in Alzheimer's disease. , 2002, Biochemical and biophysical research communications.

[65]  M. Katze,et al.  Control of PERK eIF2α kinase activity by the endoplasmic reticulum stress-induced molecular chaperone P58IPK , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[66]  B. Hyman,et al.  Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease. , 2002, Archives of neurology.

[67]  C. Masters,et al.  Increased expression of the amyloid precursor β‐secretase in Alzheimer's disease , 2002 .

[68]  Sangram S. Sisodia,et al.  γ-Secretase, notch, Aβ and alzheimer's disease: Where do the presenilins fit in? , 2002, Nature Reviews Neuroscience.

[69]  M. Staufenbiel,et al.  Expression of human β‐secretase in the mouse brain increases the steady‐state level of β‐amyloid , 2002 .

[70]  Caine W. Wong,et al.  Altered Metabolism of the Amyloid β Precursor Protein Is Associated with Mitochondrial Dysfunction in Down's Syndrome , 2002, Neuron.

[71]  Amy S. Lee,et al.  The glucose-regulated proteins: stress induction and clinical applications. , 2001, Trends in biochemical sciences.

[72]  T. Tabira,et al.  Three novel alternatively spliced isoforms of the human beta-site amyloid precursor protein cleaving enzyme (BACE) and their effect on amyloid beta-peptide production , 2001, Neuroscience Letters.

[73]  E McEwen,et al.  Translational control is required for the unfolded protein response and in vivo glucose homeostasis. , 2001, Molecular cell.

[74]  D. Ron,et al.  Diabetes mellitus and exocrine pancreatic dysfunction in perk-/- mice reveals a role for translational control in secretory cell survival. , 2001, Molecular cell.

[75]  D. Ron,et al.  Feedback Inhibition of the Unfolded Protein Response by GADD34-Mediated Dephosphorylation of eIF2α , 2001, The Journal of cell biology.

[76]  W. Richards,et al.  Mice deficient in BACE1, the Alzheimer's β-secretase, have normal phenotype and abolished β-amyloid generation , 2001, Nature Neuroscience.

[77]  R. Doms,et al.  Maturation and Endosomal Targeting of β-Site Amyloid Precursor Protein-cleaving Enzyme , 2000, The Journal of Biological Chemistry.

[78]  V. Katta,et al.  Characterization of Alzheimer's beta -secretase protein BACE. A pepsin family member with unusual properties. , 2000 .

[79]  G. Rao Oxidant Stress Stimulates Phosphorylation of eIF4E without an Effect on Global Protein Synthesis in Smooth Muscle Cells , 2000, The Journal of Biological Chemistry.

[80]  J. Tang,et al.  Human aspartic protease memapsin 2 cleaves the beta-secretase site of beta-amyloid precursor protein. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[81]  R. Sood,et al.  A mammalian homologue of GCN2 protein kinase important for translational control by phosphorylation of eukaryotic initiation factor-2alpha. , 2000, Genetics.

[82]  Stanley I. Rapoport,et al.  In vivo PET imaging and postmortem studies suggest potentially reversible and irreversible stages of brain metabolic failure in Alzheimer’s disease , 1999, European Archives of Psychiatry and Clinical Neuroscience.

[83]  Alfredo G. Tomasselli,et al.  Membrane-anchored aspartyl protease with Alzheimer's disease β-secretase activity , 1999, Nature.

[84]  R. Barbour,et al.  Purification and cloning of amyloid precursor protein β-secretase from human brain , 1999, Nature.

[85]  S. Rapoport,et al.  Functional Brain Imaging in the Resting State and during Activation in Alzheimer's Disease: Implications for Disease Mechanisms Involving Oxidative Phosphorylation , 1999, Annals of the New York Academy of Sciences.

[86]  J. Treanor,et al.  Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE. , 1999, Science.

[87]  S. Mitchell Extrapyramidal features in Alzheimer's disease. , 1999, Age and ageing.

[88]  D. Ron,et al.  Protein translation and folding are coupled by an endoplasmic-reticulum-resident kinase , 1999, Nature.

[89]  S. Younkin The role of Aβ42 in Alzheimer's disease , 1998, Journal of Physiology-Paris.

[90]  G. Binetti,et al.  Effect of energy shortage and oxidative stress on amyloid precursor protein metabolism in COS cells , 1997, Neuroscience Letters.

[91]  S. Younkin,et al.  Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice , 1996, Science.

[92]  M. Mattson,et al.  PDGFs protect hippocampal neurons against energy deprivation and oxidative injury: evidence for induction of antioxidant pathways , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[93]  Laurie A. Miller,et al.  Senile plaques in temporal lobe epilepsy , 1994, Acta Neuropathologica.

[94]  C. R. Vázquez de Aldana,et al.  Mutations in the alpha subunit of eukaryotic translation initiation factor 2 (eIF-2 alpha) that overcome the inhibitory effect of eIF-2 alpha phosphorylation on translation initiation. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[95]  A. Hinnebusch,et al.  A protein complex of translational regulators of GCN4 mRNA is the guanine nucleotide-exchange factor for translation initiation factor 2 in yeast. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[96]  D. Selkoe,et al.  Mutation of the β-amyloid precursor protein in familial Alzheimer's disease increases β-protein production , 1992, Nature.

[97]  M. Beal,et al.  Does impairment of energy metabolism result in excitotoxic neuronal death in neurodegenerative illnesses? , 1992, Annals of neurology.

[98]  K. Struhl The DNA-binding domains of the jun oncoprotein and the yeast GCN4 transcriptional activator protein are functionally homologous , 1987, Cell.

[99]  R. Doolittle,et al.  Homology between the DNA-binding domain of the GCN4 regulatory protein of yeast and the carboxyl-terminal region of a protein coded for by the oncogene jun. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[100]  B. Reisberg,et al.  Positron emission tomographic studies of aging and Alzheimer disease. , 1983, AJNR. American journal of neuroradiology.

[101]  J. Hardy,et al.  The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics , 2009 .

[102]  M. Zile,et al.  Selective translation of mRNAs in the left ventricular myocardium of the mouse in response to acute pressure overload. , 2008, Journal of molecular and cellular cardiology.

[103]  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.

[104]  R. Tanzi,et al.  Depletion of GGA3 stabilizes BACE and enhances beta-secretase activity. , 2007, Neuron.

[105]  R. Kaufman,et al.  Divergent roles of IRE1alpha and PERK in the unfolded protein response. , 2006, Current molecular medicine.

[106]  Kai Long,et al.  A selective inhibitor of eIF2alpha dephosphorylation protects cells from ER stress. , 2005, Science.

[107]  J. Wands,et al.  Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer's disease--is this type 3 diabetes? , 2005, Journal of Alzheimer's disease : JAD.

[108]  H. Cai,et al.  Amyloid beta peptide load is correlated with increased beta-secretase activity in sporadic Alzheimer's disease patients. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[109]  T. V. Van Dooren,et al.  β-Site Amyloid Precursor Protein Cleaving Enzyme 1 Increases Amyloid Deposition in Brain Parenchyma but Reduces Cerebrovascular Amyloid Angiopathy in Aging BACE × APP[V717I] Double-Transgenic Mice , 2004 .

[110]  J. Simpkins,et al.  Increased beta-secretase activity and expression in rats following transient cerebral ischemia. , 2004, Brain research.

[111]  Bryan Maloney,et al.  Gene structure and organization of the human beta-secretase (BACE) promoter. , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[112]  S. Younkin,et al.  Altered amyloid-beta metabolism and deposition in genomic-based beta-secretase transgenic mice. , 2004, The Journal of biological chemistry.

[113]  P. Wong,et al.  Elevated β-secretase expression and enzymatic activity detected in sporadic Alzheimer disease , 2003, Nature Medicine.

[114]  B. de Strooper,et al.  Aph-1, Pen-2, and Nicastrin with Presenilin generate an active gamma-Secretase complex. , 2003, Neuron.

[115]  C. Masters,et al.  Increased expression of the amyloid precursor beta-secretase in Alzheimer's disease. , 2002, Annals of neurology.

[116]  P. S. St George-Hyslop,et al.  gamma-Secretase, Notch, Abeta and Alzheimer's disease: where do the presenilins fit in? , 2002, Nature reviews. Neuroscience.

[117]  M. Staufenbiel,et al.  Expression of human beta-secretase in the mouse brain increases the steady-state level of beta-amyloid. , 2002, Journal of neurochemistry.

[118]  M. Clemens Initiation factor eIF2 alpha phosphorylation in stress responses and apoptosis. , 2001, Progress in molecular and subcellular biology.

[119]  M. Clemens Initiation Factor eIF2α Phosphorylation in Stress Responses and Apoptosis , 2001 .

[120]  C. Proud,et al.  Regulation of eukaryotic initiation factor eIF2B. , 2001, Progress in molecular and subcellular biology.

[121]  W. Richards,et al.  Mice deficient in BACE1, the Alzheimer's beta-secretase, have normal phenotype and abolished beta-amyloid generation. , 2001, Nature neuroscience.

[122]  R. Doms,et al.  Maturation and endosomal targeting of beta-site amyloid precursor protein-cleaving enzyme. The Alzheimer's disease beta-secretase. , 2000, The Journal of biological chemistry.

[123]  C. Southan,et al.  Identification of a novel aspartic protease (Asp 2) as beta-secretase. , 1999, Molecular and cellular neurosciences.

[124]  S. Younkin The role of A beta 42 in Alzheimer's disease. , 1998, Journal of physiology, Paris.

[125]  P. Francis,et al.  The effects of perturbed energy metabolism on the processing of amyloid precursor protein in PC12 cells , 1998, Journal of Neural Transmission.

[126]  G. Glenner,et al.  Alzheimer's disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. , 1984, Biochemical and biophysical research communications.

[127]  Rena Li,et al.  Amyloid (cid:1) peptide load is correlated with increased (cid:1) -secretase activity in sporadic Alzheimer’s disease patients , 2004 .