Phosphorylation of the Translation Initiation Factor eIF2α Increases BACE1 Levels and Promotes Amyloidogenesis
暂无分享,去创建一个
D. Bennett | S. Hébert | B. Strooper | R. Vassar | C. Haass | S. Lichtenthaler | Brian D. Hitt | R. A. Velliquette | Tracy O'Connor | S. L. Cole | Erika Maus | Sébastien S. Hébert | William A. Eimer | S. Lammich | Jie Zhao | K. Sadleir | L. A. Bembinster | S. Cole | Sarah L. Cole | Katherine R. Sadleir | Rodney A Velliquette | D. Bennett
[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,et al. 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 .