Proteases and Proteolysis in Alzheimer Disease: A Multifactorial View on the Disease Process
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[1] B. Strooper,et al. Analysis of the γ-secretase interactome and validation of its association with tetraspanin-enriched microdomains , 2009, Nature Cell Biology.
[2] Y. Ihara,et al. γ-Secretase: Successive Tripeptide and Tetrapeptide Release from the Transmembrane Domain of β-Carboxyl Terminal Fragment , 2009, The Journal of Neuroscience.
[3] S. Love,et al. Neprilysin and Insulin-Degrading Enzyme Levels Are Increased in Alzheimer Disease in Relation to Disease Severity , 2009, Journal of neuropathology and experimental neurology.
[4] S. Love,et al. Endothelin-converting enzyme-2 is increased in Alzheimer's disease and up-regulated by Abeta. , 2009, The American journal of pathology.
[5] F. Fahrenholz,et al. Up‐regulation of the α‐secretase ADAM10 by retinoic acid receptors and acitretin , 2009, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[6] R. D'Hooge,et al. γ-Secretase Heterogeneity in the Aph1 Subunit: Relevance for Alzheimer’s Disease , 2009, Science.
[7] B. de Strooper,et al. ADAM10, the Rate-limiting Protease of Regulated Intramembrane Proteolysis of Notch and Other Proteins, Is Processed by ADAMS-9, ADAMS-15, and the γ-Secretase* , 2009, Journal of Biological Chemistry.
[8] B. Roques,et al. Aminopeptidase A contributes to the N‐terminal truncation of amyloid β‐peptide , 2009, Journal of neurochemistry.
[9] N. Seeds,et al. Plasminogen activator activity is inhibited while neuroserpin is up‐regulated in the Alzheimer disease brain , 2009, Journal of neurochemistry.
[10] B. de Strooper,et al. Structure and function of gamma-secretase. , 2009, Seminars in cell & developmental biology.
[11] S. Hébert,et al. Alterations of the microRNA network cause neurodegenerative disease , 2009, Trends in Neurosciences.
[12] K. Horiuchi,et al. ADAMs 10 and 17 represent differentially regulated components of a general shedding machinery for membrane proteins such as transforming growth factor alpha, L-selectin, and tumor necrosis factor alpha. , 2009, Molecular biology of the cell.
[13] P. Campochiaro,et al. ADAM9 Is Involved in Pathological Retinal Neovascularization , 2009, Molecular and Cellular Biology.
[14] D. Teplow,et al. Amyloid β-Protein Assembly and Alzheimer Disease* , 2009, Journal of Biological Chemistry.
[15] Marc Tessier-Lavigne,et al. APP binds DR6 to trigger axon pruning and neuron death via distinct caspases , 2009, Nature.
[16] B. De Strooper,et al. The Orphan G Protein–Coupled Receptor 3 Modulates Amyloid-Beta Peptide Generation in Neurons , 2009, Science.
[17] A. Sun,et al. Truncated tau at D421 is associated with neurodegeneration and tangle formation in the brain of Alzheimer transgenic models , 2009, Acta Neuropathologica.
[18] B. Strooper,et al. Alzheimer's dementia by circulation disorders: when trees hide the forest , 2009, Nature Cell Biology.
[19] R. Deane,et al. SRF and myocardin regulate LRP-mediated amyloid-β clearance in brain vascular cells , 2009, Nature Cell Biology.
[20] J. McLaurin,et al. Selective targeting of perivascular macrophages for clearance of β-amyloid in cerebral amyloid angiopathy , 2009, Proceedings of the National Academy of Sciences.
[21] I. Plante,et al. MicroRNA-298 and MicroRNA-328 Regulate Expression of Mouse β-Amyloid Precursor Protein-converting Enzyme 1* , 2009, Journal of Biological Chemistry.
[22] Birgit Dümpelfeld,et al. Purification, pharmacological modulation, and biochemical characterization of interactors of endogenous human gamma-secretase. , 2009, Biochemistry.
[23] D. Selkoe,et al. Cryoelectron microscopy structure of purified gamma-secretase at 12 A resolution. , 2009, Journal of molecular biology.
[24] M. Leissring,et al. Insulin-degrading enzyme is exported via an unconventional protein secretion pathway , 2009, Molecular Neurodegeneration.
[25] Alison R. Gregro,et al. First Demonstration of Cerebrospinal Fluid and Plasma Aβ Lowering with Oral Administration of a β-Site Amyloid Precursor Protein-Cleaving Enzyme 1 Inhibitor in Nonhuman Primates , 2009, Journal of Pharmacology and Experimental Therapeutics.
[26] D. Bennett,et al. Phosphorylation of the Translation Initiation Factor eIF2α Increases BACE1 Levels and Promotes Amyloidogenesis , 2008, Neuron.
[27] Alberto Pupi,et al. Brain Glucose Hypometabolism and Oxidative Stress in Preclinical Alzheimer's Disease , 2008, Annals of the New York Academy of Sciences.
[28] V. Lee,et al. Effects of TNFα-Converting Enzyme Inhibition on Amyloid β Production and APP Processing In Vitro and In Vivo , 2008, The Journal of Neuroscience.
[29] F. Gage,et al. Long-term neprilysin gene transfer is associated with reduced levels of intracellular Abeta and behavioral improvement in APP transgenic mice , 2008, BMC Neuroscience.
[30] Jeffrey A. James,et al. Frequent amyloid deposition without significant cognitive impairment among the elderly. , 2008, Archives of neurology.
[31] L. Gan,et al. Cystatin C-Cathepsin B Axis Regulates Amyloid Beta Levels and Associated Neuronal Deficits in an Animal Model of Alzheimer's Disease , 2008, Neuron.
[32] B. Hyman,et al. Serum cystatin C and the risk of Alzheimer disease in elderly men , 2008, Neurology.
[33] Hans-Ulrich Demuth,et al. Glutaminyl cyclase inhibition attenuates pyroglutamate Aβ and Alzheimer's disease–like pathology , 2008, Nature Medicine.
[34] D. Selkoe,et al. Direct and Potent Regulation of γ-Secretase by Its Lipid Microenvironment* , 2008, Journal of Biological Chemistry.
[35] T. Hoffmann,et al. Isoaspartate-containing amyloid precursor protein-derived peptides alter efficacy and specificity of potential β-secretases , 2008, Biological chemistry.
[36] H. Demuth,et al. Alternative pathways for production of β-amyloid peptides of Alzheimer's disease , 2008, Biological chemistry.
[37] T. Hoffmann,et al. Isoaspartate residues dramatically influence substrate recognition and turnover by proteases , 2008, Biological chemistry.
[38] B. Trapp,et al. Genetic deletion of BACE1 in mice affects remyelination of sciatic nerves , 2008, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[39] T. Hoffmann,et al. Inhibition of glutaminyl cyclase prevents pGlu‐Aβ formation after intracortical/hippocampal microinjection in vivo/in situ , 2008, Journal of neurochemistry.
[40] B. de Strooper,et al. Presenilins: members of the gamma-secretase quartets, but part-time soloists too. , 2008, Physiology.
[41] Shaomin Li,et al. Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory , 2008, Nature Medicine.
[42] Seth Love,et al. Long-term effects of Aβ42 immunisation in Alzheimer's disease: follow-up of a randomised, placebo-controlled phase I trial , 2008, The Lancet.
[43] P. Wong,et al. Glu332 in the Nicastrin Ectodomain Is Essential for γ-Secretase Complex Maturation but Not for Its Activity* , 2008, Journal of Biological Chemistry.
[44] R. D'Hooge,et al. Deficiency of Aph1B/C-γ-secretase disturbs Nrg1 cleavage and sensorimotor gating that can be reversed with antipsychotic treatment , 2008, Proceedings of the National Academy of Sciences.
[45] B. de Strooper,et al. Transmembrane Domain 9 of Presenilin Determines the Dynamic Conformation of the Catalytic Site of γ-Secretase* , 2008, Journal of Biological Chemistry.
[46] M. Wolfe,et al. Promotion of BACE1 mRNA Alternative Splicing Reduces Amyloid β-Peptide Production* , 2008, Journal of Biological Chemistry.
[47] Ralph A. Nixon,et al. Autophagy Induction and Autophagosome Clearance in Neurons: Relationship to Autophagic Pathology in Alzheimer's Disease , 2008, The Journal of Neuroscience.
[48] E. Mandelkow,et al. Tau-based treatment strategies in neurodegenerative diseases , 2008, Neurotherapeutics.
[49] T. Morgan,et al. Expression of a noncoding RNA is elevated in Alzheimer's disease and drives rapid feed-forward regulation of β-secretase , 2008, Nature Medicine.
[50] M. Ciotti,et al. Identification of a caspase-derived N-terminal tau fragment in cellular and animal Alzheimer's disease models , 2008, Molecular and Cellular Neuroscience.
[51] T. Comery,et al. Enhanced clearance of Aβ in brain by sustaining the plasmin proteolysis cascade , 2008, Proceedings of the National Academy of Sciences.
[52] M. Wolfe,et al. Substrate-targeting γ-secretase modulators , 2008, Nature.
[53] T. Iwatsubo,et al. The C-Terminal PAL Motif and Transmembrane Domain 9 of Presenilin 1 Are Involved in the Formation of the Catalytic Pore of the γ-Secretase , 2008, The Journal of Neuroscience.
[54] Brian Spencer,et al. The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice. , 2008, The Journal of clinical investigation.
[55] R. Nixon,et al. Neurodegenerative lysosomal disorders: A continuum from development to late age , 2008, Autophagy.
[56] E. Malito,et al. Amyloid β-degrading cryptidases: insulin degrading enzyme, presequence peptidase, and neprilysin , 2008, Cellular and Molecular Life Sciences.
[57] F. García-Sierra,et al. Accumulation of Aspartic Acid421- and Glutamic Acid391-Cleaved Tau in Neurofibrillary Tangles Correlates With Progression in Alzheimer Disease , 2008, Journal of neuropathology and experimental neurology.
[58] 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.
[59] J. Schulz,et al. Efficient Inhibition of the Alzheimer's Disease β-Secretase by Membrane Targeting , 2008, Science.
[60] D. Price,et al. Alteration of BACE1-dependent NRG1/ErbB4 signaling and schizophrenia-like phenotypes in BACE1-null mice , 2008, Proceedings of the National Academy of Sciences.
[61] S. Love,et al. MMP‐2, ‐3 and ‐9 levels and activity are not related to Aβ load in the frontal cortex in Alzheimer's disease , 2008, Neuropathology and applied neurobiology.
[62] M. Kindy,et al. Inhibitors of Cathepsin B Improve Memory and Reduce β-Amyloid in Transgenic Alzheimer Disease Mice Expressing the Wild-type, but Not the Swedish Mutant, β-Secretase Site of the Amyloid Precursor Protein* , 2008, Journal of Biological Chemistry.
[63] Bryan Maloney,et al. Transcriptional Regulation of β-Secretase by p25/cdk5 Leads to Enhanced Amyloidogenic Processing , 2008, Neuron.
[64] A. Simon,et al. In Vivo β-Secretase 1 Inhibition Leads to Brain Aβ Lowering and Increased α-Secretase Processing of Amyloid Precursor Protein without Effect on Neuregulin-1 , 2008, Journal of Pharmacology and Experimental Therapeutics.
[65] Richard I. Morimoto,et al. Adapting Proteostasis for Disease Intervention , 2008, Science.
[66] 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.
[67] H. Bujard,et al. The Potential for β-Structure in the Repeat Domain of Tau Protein Determines Aggregation, Synaptic Decay, Neuronal Loss, and Coassembly with Endogenous Tau in Inducible Mouse Models of Tauopathy , 2008, The Journal of Neuroscience.
[68] R. Schekman,et al. Biogenesis of γ-secretase early in the secretory pathway , 2007, The Journal of cell biology.
[69] M. Staufenbiel,et al. Cystatin C modulates cerebral β-amyloidosis , 2007, Nature Genetics.
[70] D. Radvinsky,et al. Cystatin C inhibits amyloid-β deposition in Alzheimer's disease mouse models , 2007, Nature Genetics.
[71] D. Schenk,et al. Amyloid β-Protein Precursor Juxtamembrane Domain Regulates Specificity of γ-Secretase-dependent Cleavages* , 2007, Journal of Biological Chemistry.
[72] J. Marth,et al. β-Galactoside α2,6-Sialyltransferase I Cleavage by BACE1 Enhances the Sialylation of Soluble Glycoproteins , 2007, Journal of Biological Chemistry.
[73] B. de Strooper,et al. Active γ-Secretase Complexes Contain Only One of Each Component* , 2007, Journal of Biological Chemistry.
[74] Paul Maruff,et al. β-amyloid imaging and memory in non-demented individuals: evidence for preclinical Alzheimer's disease , 2007 .
[75] S. Bandyopadhyay,et al. Role of the APP non-amyloidogenic signaling pathway and targeting alpha-secretase as an alternative drug target for treatment of Alzheimer's disease. , 2007, Current medicinal chemistry.
[76] Manuel Buttini,et al. Partial Reduction of BACE1 Has Dramatic Effects on Alzheimer Plaque and Synaptic Pathology in APP Transgenic Mice* , 2007, Journal of Biological Chemistry.
[77] J. Trojanowski,et al. Tau-mediated neurodegeneration in Alzheimer's disease and related disorders , 2007, Nature Reviews Neuroscience.
[78] T. Dang,et al. Gamma-secretase inhibitor prevents Notch3 activation and reduces proliferation in human lung cancers. , 2007, Cancer research.
[79] Rena Li,et al. Deletion of tumor necrosis factor death receptor inhibits amyloid β generation and prevents learning and memory deficits in Alzheimer's mice , 2007, The Journal of Cell Biology.
[80] Dong Hou Kim,et al. Upregulation of tPA/plasminogen proteolytic system in the periphery of amyloid deposits in the Tg2576 mouse model of Alzheimer's disease , 2007, Neuroscience Letters.
[81] K. Zou,et al. Angiotensin-Converting Enzyme Converts Amyloid β-Protein 1–42 (Aβ1–42) to Aβ1–40, and Its Inhibition Enhances Brain Aβ Deposition , 2007, The Journal of Neuroscience.
[82] C. Haass,et al. Endoplasmic reticulum retention of the γ‐secretase complex component Pen2 by Rer1 , 2007 .
[83] M. Korte,et al. The Secreted β-Amyloid Precursor Protein Ectodomain APPsα Is Sufficient to Rescue the Anatomical, Behavioral, and Electrophysiological Abnormalities of APP-Deficient Mice , 2007, The Journal of Neuroscience.
[84] E. Kremmer,et al. Pathological activity of familial Alzheimer’s disease-associated mutant presenilin can be executed by six different γ-secretase complexes , 2007, Neurobiology of Disease.
[85] E. Mandelkow,et al. Stepwise proteolysis liberates tau fragments that nucleate the Alzheimer-like aggregation of full-length tau in a neuronal cell model , 2007, Proceedings of the National Academy of Sciences.
[86] R. Tanzi,et al. Depletion of GGA3 Stabilizes BACE and Enhances β-Secretase Activity , 2007, Neuron.
[87] Michael P. Mazanetz,et al. Untangling tau hyperphosphorylation in drug design for neurodegenerative diseases , 2007, Nature Reviews Drug Discovery.
[88] L. Mucke,et al. Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model , 2007, Science.
[89] B. de Strooper,et al. Familial Alzheimer disease-linked mutations specifically disrupt Ca2+ leak function of presenilin 1. , 2007, The Journal of clinical investigation.
[90] D. Holtzman,et al. Transport Pathways for Clearance of Human Alzheimer's Amyloid β-Peptide and Apolipoproteins E and J in the Mouse Central Nervous System , 2007, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[91] J. Perez-polo,et al. Differential regulation of BACE1 promoter activity by nuclear factor‐κB in neurons and glia upon exposure to β‐amyloid peptides , 2007 .
[92] M. Hentze,et al. Complex translational regulation of BACE1 involves upstream AUGs and stimulatory elements within the 5′ untranslated region , 2007, Nucleic acids research.
[93] Jiankun Cui,et al. Hypoxia-inducible Factor 1 (HIF-1 )-mediated Hypoxia Increases BACE1 Expression and -Amyloid Generation* , 2007 .
[94] D. Selkoe,et al. Effects of prolonged angiotensin-converting enzyme inhibitor treatment on amyloid β-protein metabolism in mouse models of Alzheimer disease , 2007, Neurobiology of Disease.
[95] Dieter Langosch,et al. GxxxG motifs within the amyloid precursor protein transmembrane sequence are critical for the etiology of Aβ42 , 2007 .
[96] D. Spasic,et al. Rer1p competes with APH-1 for binding to nicastrin and regulates γ-secretase complex assembly in the early secretory pathway , 2007, The Journal of cell biology.
[97] B. Strooper. Loss-of-function presenilin mutations in Alzheimer disease. Talking Point on the role of presenilin mutations in Alzheimer disease. , 2007 .
[98] D. Selkoe,et al. Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide , 2007, Nature Reviews Molecular Cell Biology.
[99] N. Zilka,et al. Neurodegeneration caused by expression of human truncated tau leads to progressive neurobehavioural impairment in transgenic rats , 2007, Brain Research.
[100] A. Sehara-Fujisawa,et al. ADAM19 is tightly associated with constitutive alzheimer's disease APP α-secretase in A172 cells , 2007 .
[101] E. Mandelkow,et al. Structural Principles of Tau and the Paired Helical Filaments of Alzheimer’s Disease , 2007, Brain pathology.
[102] M. Famulok,et al. GGA1 Is Expressed in the Human Brain and Affects the Generation of Amyloid β-Peptide , 2006, The Journal of Neuroscience.
[103] R. Hepler,et al. Solution State Characterization of Amyloid β-Derived Diffusible Ligands , 2006 .
[104] Hong Qing,et al. Hypoxia facilitates Alzheimer's disease pathogenesis by up-regulating BACE1 gene expression , 2006, Proceedings of the National Academy of Sciences.
[105] Yun Bai,et al. Activation of β2-adrenergic receptor stimulates γ-secretase activity and accelerates amyloid plaque formation , 2006, Nature Medicine.
[106] K. Kosik. The neuronal microRNA system , 2006, Nature Reviews Neuroscience.
[107] P. Wong,et al. Bace1 modulates myelination in the central and peripheral nervous system , 2006, Nature Neuroscience.
[108] T. Iwatsubo,et al. Structure of the Catalytic Pore of γ-Secretase Probed by the Accessibility of Substituted Cysteines , 2006, The Journal of Neuroscience.
[109] P. Saftig,et al. Control of Peripheral Nerve Myelination by the ß-Secretase BACE1 , 2006, Science.
[110] D. Holtzman,et al. Matrix Metalloproteinases Expressed by Astrocytes Mediate Extracellular Amyloid-β Peptide Catabolism , 2006, The Journal of Neuroscience.
[111] Jiyeon Lee,et al. Furin is an endogenous regulator of α-secretase associated APP processing , 2006 .
[112] C. Eckman,et al. Regulation of Steady-state β-Amyloid Levels in the Brain by Neprilysin and Endothelin-converting Enzyme but Not Angiotensin-converting Enzyme* , 2006, Journal of Biological Chemistry.
[113] L. Tjernberg,et al. Degradation of the Amyloid β-Protein by the Novel Mitochondrial Peptidasome, PreP*♦ , 2006, Journal of Biological Chemistry.
[114] R. Berry,et al. N-terminal fragments of tau inhibit full-length tau polymerization in vitro. , 2006, Biochemistry.
[115] L. Mucke,et al. Antiamyloidogenic and Neuroprotective Functions of Cathepsin B: Implications for Alzheimer's Disease , 2006, Neuron.
[116] B. de Strooper,et al. Contribution of Presenilin Transmembrane Domains 6 and 7 to a Water-containing Cavity in the γ-Secretase Complex* , 2006, Journal of Biological Chemistry.
[117] B. Strooper,et al. Presenilins Form ER Ca2+ Leak Channels, a Function Disrupted by Familial Alzheimer's Disease-Linked Mutations , 2006, Cell.
[118] D. Geschwind,et al. A Genomic Screen for Modifiers of Tauopathy Identifies Puromycin-Sensitive Aminopeptidase as an Inhibitor of Tau-Induced Neurodegeneration , 2006, Neuron.
[119] Jin-Moo Lee,et al. Matrix Metalloproteinase-9 Degrades Amyloid-β Fibrils in Vitro and Compact Plaques in Situ* , 2006, Journal of Biological Chemistry.
[120] S. Hébert,et al. Regulated intramembrane proteolysis of amyloid precursor protein and regulation of expression of putative target genes , 2006, EMBO reports.
[121] P. Filipcik,et al. Truncated tau from sporadic Alzheimer's disease suffices to drive neurofibrillary degeneration in vivo , 2006, FEBS letters.
[122] David M Holtzman,et al. Human amyloid-β synthesis and clearance rates as measured in cerebrospinal fluid in vivo , 2006, Nature Medicine.
[123] M. Sastre,et al. Transcriptional and translational regulation of BACE1 expression—Implications for Alzheimer's disease , 2006, Progress in Neurobiology.
[124] J. Trojanowski,et al. Characterization of Aβ11-40/42 peptide deposition in Alzheimer’s disease and young Down’s syndrome brains: implication of N-terminally truncated Aβ species in the pathogenesis of Alzheimer’s disease , 2006, Acta Neuropathologica.
[125] Y. Ihara,et al. Equimolar Production of Amyloid β-Protein and Amyloid Precursor Protein Intracellular Domain from β-Carboxyl-terminal Fragment by γ-Secretase* , 2006, Journal of Biological Chemistry.
[126] Weihui Zhou,et al. Leaky Scanning and Reinitiation Regulate BACE1 Gene Expression , 2006, Alzheimer's & Dementia.
[127] J. Vickers,et al. No difference in expression of apoptosis-related proteins and apoptotic morphology in control, pathologically aged and Alzheimer's disease cases , 2006, Neurobiology of Disease.
[128] M. Gallagher,et al. A specific amyloid-β protein assembly in the brain impairs memory , 2006, Nature.
[129] Y. Ihara,et al. DAPT-Induced Intracellular Accumulations of Longer Amyloid β-Proteins: Further Implications for the Mechanism of Intramembrane Cleavage by γ-Secretase† , 2006 .
[130] Gina N. LaRossa,et al. Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Aβ42 in humans , 2006, Annals of neurology.
[131] B. Strooper,et al. Presenilin clinical mutations can affect γ‐secretase activity by different mechanisms , 2006, Journal of neurochemistry.
[132] H. Steinhoff,et al. Global hairpin folding of tau in solution. , 2006, Biochemistry.
[133] N. Ostermann,et al. Crystal structure of human BACE2 in complex with a hydroxyethylamine transition-state inhibitor. , 2006, Journal of molecular biology.
[134] E. Mandelkow,et al. Inducible Expression of Tau Repeat Domain in Cell Models of Tauopathy , 2006, Journal of Biological Chemistry.
[135] J. Kuret,et al. C‐terminal truncation modulates both nucleation and extension phases of τ fibrillization , 2006, FEBS letters.
[136] 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.
[137] S. Hébert,et al. The amyloid‐β precursor protein: integrating structure with biological function , 2005 .
[138] P. Krawitz,et al. Differential Localization and Identification of a Critical Aspartate Suggest Non-redundant Proteolytic Functions of the Presenilin Homologues SPPL2b and SPPL3* , 2005, Journal of Biological Chemistry.
[139] 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.
[140] Yunzhou Dong,et al. γ-Cleavage Is Dependent on ζ-Cleavage during the Proteolytic Processing of Amyloid Precursor Protein within Its Transmembrane Domain* , 2005, Journal of Biological Chemistry.
[141] L. Tjernberg,et al. Macroautophagy—a novel β-amyloid peptide-generating pathway activated in Alzheimer's disease , 2005, The Journal of cell biology.
[142] A. Gliozzi,et al. β-Amyloid Is Different in Normal Aging and in Alzheimer Disease* , 2005, Journal of Biological Chemistry.
[143] B. Hyman,et al. APP substitutions V715F and L720P alter PS1 conformation and differentially affect Aβ and AICD generation , 2005, Journal of neurochemistry.
[144] B. Hyman,et al. BACE Is Degraded via the Lysosomal Pathway* , 2005, Journal of Biological Chemistry.
[145] Rudi D'Hooge,et al. Phenotypic and Biochemical Analyses of BACE1- and BACE2-deficient Mice* , 2005, Journal of Biological Chemistry.
[146] Y. Matsuoka,et al. Biological significance of isoaspartate and its repair system. , 2005, Biological & pharmaceutical bulletin.
[147] B. Ghetti,et al. Amino-terminally truncated Abeta peptide species are the main component of cotton wool plaques. , 2005, Biochemistry.
[148] T. Südhof,et al. Nicastrin Functions as a γ-Secretase-Substrate Receptor , 2005, Cell.
[149] J. Hardy,et al. Aβ42 Is Essential for Parenchymal and Vascular Amyloid Deposition in Mice , 2005, Neuron.
[150] Christian Griesinger,et al. Sites of Tau Important for Aggregation Populate β-Structure and Bind to Microtubules and Polyanions* , 2005, Journal of Biological Chemistry.
[151] B. de Strooper,et al. ADAM10 mediates E-cadherin shedding and regulates epithelial cell-cell adhesion, migration, and beta-catenin translocation. , 2005, Proceedings of the National Academy of Sciences of the United States of America.
[152] R. Rozmahel,et al. Dissociated phenotypes in presenilin transgenic mice define functionally distinct γ-secretases , 2005 .
[153] B. de Strooper,et al. β Subunits of Voltage-gated Sodium Channels Are Novel Substrates of β-Site Amyloid Precursor Protein-cleaving Enzyme (BACE1) and γ-Secretase* , 2005, Journal of Biological Chemistry.
[154] Hans Clevers,et al. Notch/γ-secretase inhibition turns proliferative cells in intestinal crypts and adenomas into goblet cells , 2005, Nature.
[155] Adriana B Ferreira,et al. The Generation of a 17 kDa Neurotoxic Fragment: An Alternative Mechanism by which Tau Mediates β-Amyloid-Induced Neurodegeneration , 2005, The Journal of Neuroscience.
[156] F. Liu,et al. Post-translational modifications of tau protein in Alzheimer’s disease , 2005, Journal of Neural Transmission.
[157] B. Hyman,et al. The Low Density Lipoprotein Receptor-related Protein (LRP) Is a Novel β-Secretase (BACE1) Substrate* , 2005, Journal of Biological Chemistry.
[158] B. Strooper,et al. Erratum: ADAM10 cleavage of N-cadherin and regulation of cell-cell adhesion and β-catenin nuclear signalling (The EMBO Journal (2005) 24 (742-752)) , 2005 .
[159] Berislav V. Zlokovic,et al. Neurovascular mechanisms of Alzheimer's neurodegeneration , 2005, Trends in Neurosciences.
[160] Wanpin Chang,et al. GGA Proteins Mediate the Recycling Pathway of Memapsin 2 (BACE)* , 2005, Journal of Biological Chemistry.
[161] M. Higuchi,et al. Somatostatin regulates brain amyloid β peptide Aβ42 through modulation of proteolytic degradation , 2005, Nature Medicine.
[162] B. Hyman,et al. Familial Alzheimer's Disease Presenilin 1 Mutations Cause Alterations in the Conformation of Presenilin and Interactions with Amyloid Precursor Protein , 2005, The Journal of Neuroscience.
[163] B. de Strooper,et al. ADAM10 cleavage of N‐cadherin and regulation of cell–cell adhesion and β‐catenin nuclear signalling , 2005, The EMBO journal.
[164] E. Corder,et al. Cystatin C as a risk factor for Alzheimer disease , 2005, Neurology.
[165] P. Mcgeer,et al. Proteolysis of Non-phosphorylated and Phosphorylated Tau by Thrombin* , 2005, Journal of Biological Chemistry.
[166] D. Selkoe,et al. γ-Secretase Exists on the Plasma Membrane as an Intact Complex That Accepts Substrates and Effects Intramembrane Cleavage* , 2005, Journal of Biological Chemistry.
[167] S. Hébert,et al. Differential contribution of the three Aph1 genes to γ-secretase activity in vivo , 2005 .
[168] C. Cotman,et al. The Role of Caspase Cleavage of Tau in Alzheimer Disease Neuropathology , 2005, Journal of neuropathology and experimental neurology.
[169] Ralph A. Nixon,et al. Extensive Involvement of Autophagy in Alzheimer Disease: An Immuno-Electron Microscopy Study , 2005, Journal of neuropathology and experimental neurology.
[170] D. Price,et al. APH-1a Is the Principal Mammalian APH-1 Isoform Present in γ-Secretase Complexes during Embryonic Development , 2005, The Journal of Neuroscience.
[171] Leonid Tarassishin,et al. Processing of Notch and amyloid precursor protein by γ-secretase is spatially distinct , 2004 .
[172] S. Hébert,et al. Coordinated and widespread expression of γ-secretase in vivo: evidence for size and molecular heterogeneity , 2004, Neurobiology of Disease.
[173] A. Goate,et al. Mutations in APP have independent effects on Aβ and CTFγ generation , 2004, Neurobiology of Disease.
[174] P. Wong,et al. Association of γ-Secretase with Lipid Rafts in Post-Golgi and Endosome Membranes* , 2004, Journal of Biological Chemistry.
[175] A. Nadin,et al. Selected Non-steroidal Anti-inflammatory Drugs and Their Derivatives Target γ-Secretase at a Novel Site , 2004, Journal of Biological Chemistry.
[176] B. Hyman,et al. Demonstration of BACE (β-secretase) phosphorylation and its interaction with GGA1 in cells by fluorescence-lifetime imaging microscopy , 2004, Journal of Cell Science.
[177] Andrew P. Weng,et al. Activating Mutations of NOTCH1 in Human T Cell Acute Lymphoblastic Leukemia , 2004, Science.
[178] C. Haass,et al. Identification of Distinct γ-Secretase Complexes with Different APH-1 Variants* , 2004, Journal of Biological Chemistry.
[179] S. Younkin,et al. Plasmin deficiency does not alter endogenous murine amyloid beta levels in mice , 2004, Neuroscience Letters.
[180] Y. Ihara,et al. Truncated Carboxyl-Terminal Fragments of β-Amyloid Precursor Protein Are Processed to Amyloid β-Proteins 40 and 42† , 2004 .
[181] B. de Strooper,et al. Presenilin 1 mediates the turnover of telencephalin in hippocampal neurons via an autophagic degradative pathway , 2004, The Journal of cell biology.
[182] D. Bennett,et al. Early N-Terminal Changes and Caspase-6 Cleavage of Tau in Alzheimer's Disease , 2004, The Journal of Neuroscience.
[183] B. de Strooper,et al. Partial loss of presenilins causes seborrheic keratosis and autoimmune disease in mice. , 2004, Human molecular genetics.
[184] D. Dickson. Apoptotic mechanisms in Alzheimer neurofibrillary degeneration: cause or effect? , 2004, The Journal of clinical investigation.
[185] C. Cotman,et al. Caspase-cleavage of tau is an early event in Alzheimer disease tangle pathology. , 2004, The Journal of clinical investigation.
[186] C. Haass,et al. Expression of the Alzheimer protease BACE1 is suppressed via its 5'‐untranslated region , 2004, EMBO reports.
[187] Masahiro Shibata,et al. Insights into the Phosphoregulation of β‐Secretase Sorting Signal by the VHS Domain of GGA1 , 2004, Traffic.
[188] J. Simpkins,et al. Increased β-secretase activity and expression in rats following transient cerebral ischemia , 2004, Brain Research.
[189] E. Godaux,et al. A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model. , 2004, The Journal of clinical investigation.
[190] Christina A. Wilson,et al. Degradative organelles containing mislocalized α- and β-synuclein proliferate in presenilin-1 null neurons , 2004, The Journal of cell biology.
[191] B. Strooper,et al. Presenilins in Memory, Alzheimer's Disease, and Therapy , 2004, Neuron.
[192] M. Wolfe,et al. Signal Peptide Peptidase Forms a Homodimer That Is Labeled by an Active Site-directed γ-Secretase Inhibitor* , 2004, Journal of Biological Chemistry.
[193] T. Hoffmann,et al. Glutaminyl cyclases unfold glutamyl cyclase activity under mild acid conditions , 2004, FEBS letters.
[194] D. Selkoe,et al. Partial loss-of-function mutations in insulin-degrading enzyme that induce diabetes also impair degradation of amyloid beta-protein. , 2004, The American journal of pathology.
[195] J. Buxbaum,et al. BACE (β-secretase) modulates the processing of APLP2 in vivo , 2004, Molecular and Cellular Neuroscience.
[196] Jay S. Fine,et al. Chronic Treatment with the γ-Secretase Inhibitor LY-411,575 Inhibits β-Amyloid Peptide Production and Alters Lymphopoiesis and Intestinal Cell Differentiation* , 2004, Journal of Biological Chemistry.
[197] T. Südhof,et al. Cleavage of Amyloid-β Precursor Protein and Amyloid-β Precursor-like Protein by BACE 1* , 2004, Journal of Biological Chemistry.
[198] 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.
[199] Marija Mihailovich,et al. Translational regulation of BACE-1 expression in neuronal and non-neuronal cells. , 2004, Nucleic acids research.
[200] 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.
[201] R. Doms,et al. Membrane Topology and Nicastrin-enhanced Endoproteolysis of APH-1, a Component of the γ-Secretase Complex* , 2004, Journal of Biological Chemistry.
[202] M. Ohno,et al. BACE1 Deficiency Rescues Memory Deficits and Cholinergic Dysfunction in a Mouse Model of Alzheimer's Disease , 2004, Neuron.
[203] D. Selkoe,et al. Enhanced Proteolysis of β-Amyloid in APP Transgenic Mice Prevents Plaque Formation, Secondary Pathology, and Premature Death , 2003, Neuron.
[204] B. de Strooper,et al. The Cell Adhesion Protein P-selectin Glycoprotein Ligand-1 Is a Substrate for the Aspartyl Protease BACE1* , 2003, Journal of Biological Chemistry.
[205] W. H. Jordan,et al. Adipsin, a Biomarker of Gastrointestinal Toxicity Mediated by a Functional γ-Secretase Inhibitor* , 2003, Journal of Biological Chemistry.
[206] C. Finch,et al. Self-assembly of Aβ1-42 into globular neurotoxins , 2003 .
[207] M. Pangalos,et al. BACE1 (β-secretase) transgenic and knockout mice: identification of neurochemical deficits and behavioral changes , 2003, Molecular and Cellular Neuroscience.
[208] J. Melchor,et al. The Tissue Plasminogen Activator-Plasminogen Proteolytic Cascade Accelerates Amyloid-β (Aβ) Degradation and Inhibits Aβ-Induced Neurodegeneration , 2003, The Journal of Neuroscience.
[209] D. Riddell,et al. Characterization of the Ectodomain Shedding of the β-Site Amyloid Precursor Protein-cleaving Enzyme 1 (BACE1)* , 2003, Journal of Biological Chemistry.
[210] Tam Doan,et al. Antagonistic Effects of β-Site Amyloid Precursor Protein-cleaving Enzymes 1 and 2 on β-Amyloid Peptide Production in Cells* , 2003, Journal of Biological Chemistry.
[211] S. Weggen,et al. Evidence That Nonsteroidal Anti-inflammatory Drugs Decrease Amyloid β42 Production by Direct Modulation of γ-Secretase Activity* , 2003, Journal of Biological Chemistry.
[212] Pritam Das,et al. NSAIDs and enantiomers of flurbiprofen target γ-secretase and lower Aβ42 in vivo , 2003 .
[213] R. Berry,et al. Caspase cleavage of tau: Linking amyloid and neurofibrillary tangles in Alzheimer's disease , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[214] R. Berry,et al. Inhibition of tau polymerization by its carboxy-terminal caspase cleavage fragment. , 2003, Biochemistry.
[215] D. Aswad,et al. Deamidation and isoaspartate formation in proteins: unwanted alterations or surreptitious signals? , 2003, Cellular and Molecular Life Sciences CMLS.
[216] Min Xu,et al. Presenilin-1 and Presenilin-2 Exhibit Distinct yet Overlapping γ-Secretase Activities* , 2003, Journal of Biological Chemistry.
[217] C. Masters,et al. In vitro characterization of the presenilin-dependent gamma-secretase complex using a novel affinity ligand. , 2003, Biochemistry.
[218] T. Saido,et al. Dutch, Flemish, Italian, and Arctic mutations of APP and resistance of Aβ to physiologically relevant proteolytic degradation , 2003, The Lancet.
[219] R. Doms,et al. Membrane Topology of γ-Secretase Component PEN-2* , 2003, Journal of Biological Chemistry.
[220] Kazuyuki Takata,et al. Cdk5 Is a Key Factor in Tau Aggregation and Tangle Formation In Vivo , 2003, Neuron.
[221] T. Iwatsubo,et al. Sulindac Sulfide Is a Noncompetitive γ-Secretase Inhibitor That Preferentially Reduces Aβ42 Generation* , 2003, The Journal of Biological Chemistry.
[222] A. Schmitz,et al. Targeting Presenilin-type Aspartic Protease Signal Peptide Peptidase with γ-Secretase Inhibitors* , 2003, The Journal of Biological Chemistry.
[223] J. Schmitz,et al. γ-Secretase Activity Is Associated with a Conformational Change of Nicastrin* , 2003, The Journal of Biological Chemistry.
[224] Michael S. Wolfe,et al. γ-Secretase is a membrane protein complex comprised of presenilin, nicastrin, aph-1, and pen-2 , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[225] J. Regula,et al. Reconstitution of γ-secretase activity , 2003, Nature Cell Biology.
[226] H. Cai,et al. Nicastrin Is Required for Assembly of Presenilin/γ-Secretase Complexes to Mediate Notch Signaling and for Processing and Trafficking of β-Amyloid Precursor Protein in Mammals , 2003, The Journal of Neuroscience.
[227] B. Strooper,et al. Aph-1, Pen-2, and Nicastrin with Presenilin Generate an Active γ-Secretase Complex , 2003, Neuron.
[228] T. Iwatsubo,et al. The role of presenilin cofactors in the γ-secretase complex , 2003, Nature.
[229] R. Malinow,et al. APP Processing and Synaptic Function , 2003, Neuron.
[230] F. Gage,et al. Neprilysin Gene Transfer Reduces Human Amyloid Pathology in Transgenic Mice , 2003, The Journal of Neuroscience.
[231] Matthew P. Frosch,et al. Insulin-degrading enzyme regulates the levels of insulin, amyloid β-protein, and the β-amyloid precursor protein intracellular domain in vivo , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[232] R. Doms,et al. Secretion and Intracellular Generation of Truncated Aβ in β-Site Amyloid-β Precursor Protein-cleaving Enzyme Expressing Human Neurons* , 2003, The Journal of Biological Chemistry.
[233] B. Szabó,et al. Putative function of ADAM9, ADAM10, and ADAM17 as APP -secretase , 2003 .
[234] L. Marlow,et al. Alzheimer's Disease β-Amyloid Peptide Is Increased in Mice Deficient in Endothelin-converting Enzyme* , 2003, The Journal of Biological Chemistry.
[235] Harald Steiner,et al. Presenilin-dependent Intramembrane Proteolysis of CD44 Leads to the Liberation of Its Intracellular Domain and the Secretion of an Aβ-like Peptide* , 2002, The Journal of Biological Chemistry.
[236] Hirotaka Yoshida,et al. Abundant Tau Filaments and Nonapoptotic Neurodegeneration in Transgenic Mice Expressing Human P301S Tau Protein , 2002, The Journal of Neuroscience.
[237] T. Kudo,et al. Presenilins mediate a dual intramembranous γ‐secretase cleavage of Notch‐1 , 2002 .
[238] B. de Strooper,et al. The disintegrin/metalloprotease ADAM 10 is essential for Notch signalling but not for alpha-secretase activity in fibroblasts. , 2002, Human molecular genetics.
[239] B. Hyman,et al. Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease. , 2002, Archives of neurology.
[240] G. Damonte,et al. Pyroglutamate‐modified amyloid β‐peptides – AβN3(pE) – strongly affect cultured neuron and astrocyte survival , 2002 .
[241] G. Perry,et al. Oxidative Stress Increases Expression and Activity of BACE in NT2 Neurons , 2002, Neurobiology of Disease.
[242] Wanpin Chang,et al. Memapsin 2 (β‐secretase) cytosolic domain binds to the VHS domains of GGA1 and GGA2: implications on the endocytosis mechanism of memapsin 2 , 2002, FEBS letters.
[243] C. Masters,et al. Increased expression of the amyloid precursor β‐secretase in Alzheimer's disease , 2002 .
[244] G. Westmeyer,et al. A non‐amyloidogenic function of BACE‐2 in the secretory pathway , 2002, Journal of neurochemistry.
[245] C. Haass,et al. Insulin-degrading Enzyme Rapidly Removes the β-Amyloid Precursor Protein Intracellular Domain (AICD)* , 2002, The Journal of Biological Chemistry.
[246] W. K. Cullen,et al. Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo , 2002, Nature.
[247] M. Molinari,et al. The disulphide bonds in the catalytic domain of BACE are critical but not essential for amyloid precursor protein processing activity , 2002, Journal of neurochemistry.
[248] G. Weskamp,et al. Mice Lacking the Metalloprotease-Disintegrin MDC9 (ADAM9) Have No Evident Major Abnormalities during Development or Adult Life , 2002, Molecular and Cellular Biology.
[249] A. Igarashi,et al. Angiotensin-converting Enzyme Degrades Alzheimer Amyloid β-Peptide (Aβ); Retards Aβ Aggregation, Deposition, Fibril Formation; and Inhibits Cytotoxicity* , 2001, The Journal of Biological Chemistry.
[250] Rong Wang,et al. A subset of NSAIDs lower amyloidogenic Aβ42 independently of cyclooxygenase activity , 2001, Nature.
[251] M. Fini,et al. Effects of Matrix Metalloproteinase-9 Gene Knock-Out on the Proteolysis of Blood–Brain Barrier and White Matter Components after Cerebral Ischemia , 2001, The Journal of Neuroscience.
[252] D. Skovronsky,et al. Neuronal localization of the TNFalpha converting enzyme (TACE) in brain tissue and its correlation to amyloid plaques. , 2001, Journal of neurobiology.
[253] R. Yan,et al. BACE2 Functions as an Alternative α-Secretase in Cells* , 2001, The Journal of Biological Chemistry.
[254] B. de Strooper,et al. The amyloid precursor protein (APP)‐cytoplasmic fragment generated by γ‐secretase is rapidly degraded but distributes partially in a nuclear fraction of neurones in culture , 2001, Journal of neurochemistry.
[255] H. Vanderstichele,et al. The discrepancy between presenilin subcellular localization and γ-secretase processing of amyloid precursor protein , 2001, The Journal of cell biology.
[256] F. Fahrenholz,et al. Regulation of the α‐secretase ADAM10 by its prodomain and proprotein convertases , 2001 .
[257] Thomas C. Südhof,et al. A Transcriptively Active Complex of APP with Fe65 and Histone Acetyltransferase Tip60 , 2001, Science.
[258] C. Eckman,et al. Degradation of the Alzheimer's Amyloid β Peptide by Endothelin-converting Enzyme* , 2001, The Journal of Biological Chemistry.
[259] Gregory D. Longmore,et al. γ-Secretase inhibitors repress thymocyte development , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[260] I. Kola,et al. BACE knockout mice are healthy despite lacking the primary beta-secretase activity in brain: implications for Alzheimer's disease therapeutics. , 2001, Human molecular genetics.
[261] T. Saido,et al. Metabolic Regulation of Brain Aβ by Neprilysin , 2001, Science.
[262] G. Multhaup,et al. Phosphorylation Regulates Intracellular Trafficking of β-Secretase* , 2001, The Journal of Biological Chemistry.
[263] M. Staufenbiel,et al. Comparative Analysis of Amyloid-β Chemical Structure and Amyloid Plaque Morphology of Transgenic Mouse and Alzheimer's Disease Brains* , 2001, The Journal of Biological Chemistry.
[264] Louise Wickham,et al. Post-translational Processing of β-Secretase (β-Amyloid-converting Enzyme) and Its Ectodomain Shedding , 2001, The Journal of Biological Chemistry.
[265] H. Cai,et al. BACE1 is the major β-secretase for generation of Aβ peptides by neurons , 2001, Nature Neuroscience.
[266] N. Seidah,et al. Constitutive α‐secretase cleavage of the β‐amyloid precursor protein in the furin‐deficient LoVo cell line: involvement of the pro‐hormone convertase 7 and the disintegrin metalloprotease ADAM10 , 2001, Journal of neurochemistry.
[267] W. Richards,et al. Mice deficient in BACE1, the Alzheimer's β-secretase, have normal phenotype and abolished β-amyloid generation , 2001, Nature Neuroscience.
[268] B. de Strooper,et al. Processing of β-Secretase by Furin and Other Members of the Proprotein Convertase Family* , 2001, The Journal of Biological Chemistry.
[269] A. Delacourte,et al. Brain plasmin enhances APP α‐cleavage and Aβ degradation and is reduced in Alzheimer's disease brains , 2000 .
[270] H. Lipp,et al. Mice with Combined Gene Knock-Outs Reveal Essential and Partially Redundant Functions of Amyloid Precursor Protein Family Members , 2000, The Journal of Neuroscience.
[271] N. Seidah,et al. Coordinated Expression of β‐Amyloid Precursor Protein and the Putative β‐Secretase BACE and α‐Secretase ADAM10 in Mouse and Human Brain , 2000 .
[272] R. Doms,et al. Maturation and Endosomal Targeting of β-Site Amyloid Precursor Protein-cleaving Enzyme , 2000, The Journal of Biological Chemistry.
[273] J. Kuret,et al. Oxidative regulation of fatty acid-induced tau polymerization. , 2000, Biochemistry.
[274] L Hong,et al. Structure of the protease domain of memapsin 2 (beta-secretase) complexed with inhibitor. , 2000, Science.
[275] G. Multhaup,et al. Maturation and Pro-peptide Cleavage of β-Secretase* , 2000, The Journal of Biological Chemistry.
[276] M. Fini,et al. Effects of Matrix Metalloproteinase-9 Gene Knock-Out on Morphological and Motor Outcomes after Traumatic Brain Injury , 2000, The Journal of Neuroscience.
[277] G. Struhl,et al. Requirements for presenilin-dependent cleavage of notch and other transmembrane proteins. , 2000, Molecular cell.
[278] C. Schnitzler,et al. BACE2, a β-secretase homolog, cleaves at the β site and within the amyloid-β region of the amyloid-β precursor protein , 2000 .
[279] Patrick R. Hof,et al. Tau protein isoforms, phosphorylation and role in neurodegenerative disorders 1 1 These authors contributed equally to this work. , 2000, Brain Research Reviews.
[280] V. Katta,et al. Characterization of Alzheimer's beta -secretase protein BACE. A pepsin family member with unusual properties. , 2000 .
[281] B. Strooper,et al. Total inactivation of γ–secretase activity in presenilin-deficient embryonic stem cells , 2000, Nature Cell Biology.
[282] T. Saido,et al. Reply to: 'Clearance of amyloid β-peptide from brain: transport or metabolism?' , 2000, Nature Medicine.
[283] A. Bernstein,et al. Presenilins are required for γ-secretase cleavage of β-APP and transmembrane cleavage of Notch-1 , 2000, Nature Cell Biology.
[284] S. Scheff,et al. The Plasmin System Is Induced by and Degrades Amyloid-β Aggregates , 2000, The Journal of Neuroscience.
[285] E. Mandelkow,et al. Assembly of tau protein into Alzheimer paired helical filaments depends on a local sequence motif ((306)VQIVYK(311)) forming beta structure. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[286] D. Selkoe,et al. Neurons Regulate Extracellular Levels of Amyloid β-Protein via Proteolysis by Insulin-Degrading Enzyme , 2000, The Journal of Neuroscience.
[287] 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.
[288] T. Saido,et al. Identification of the major Aβ1–42-degrading catabolic pathway in brain parenchyma: Suppression leads to biochemical and pathological deposition , 2000, Nature Medicine.
[289] R. Barbour,et al. Purification and cloning of amyloid precursor protein β-secretase from human brain , 1999, Nature.
[290] Alfredo G. Tomasselli,et al. Membrane-anchored aspartyl protease with Alzheimer's disease β-secretase activity , 1999, Nature.
[291] David G. Tew,et al. Identification of a Novel Aspartic Protease (Asp 2) as β-Secretase , 1999, Molecular and Cellular Neuroscience.
[292] N. Seidah,et al. Proprotein Convertase Activity Contributes to the Processing of the Alzheimer's β‐Amyloid Precursor Protein in Human Cells: Evidence for a Role of the Prohormone Convertase PC7 in the Constitutive ‐Secretase Pathway , 1999, Journal of neurochemistry.
[293] A. Bernstein,et al. Mice lacking both presenilin genes exhibit early embryonic patterning defects. , 1999, Genes & development.
[294] J. Treanor,et al. Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE. , 1999, Science.
[295] B. de Strooper,et al. Presenilin 1 Controls γ-Secretase Processing of Amyloid Precursor Protein in Pre-Golgi Compartments of Hippocampal Neurons , 1999, The Journal of cell biology.
[296] K. Suzuki,et al. Membrane-anchored metalloprotease MDC9 has an alpha-secretase activity responsible for processing the amyloid precursor protein. , 1999, The Biochemical journal.
[297] H. Vanderstichele,et al. Presenilin 2 deficiency causes a mild pulmonary phenotype and no changes in amyloid precursor protein processing but enhances the embryonic lethal phenotype of presenilin 1 deficiency. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[298] B. Strooper,et al. Presenilins: molecular switches between proteolysis and signal transduction , 1999, Trends in Neurosciences.
[299] B. Dubois,et al. Early-onset autosomal dominant Alzheimer disease: prevalence, genetic heterogeneity, and mutation spectrum. , 1999, American journal of human genetics.
[300] B. Strooper,et al. Presenilin-1 deficiency leads to loss of Cajal–Retzius neurons and cortical dysplasia similar to human type 2 lissencephaly , 1999, Current Biology.
[301] R. Crowther,et al. Effects of frontotemporal dementia FTDP‐17 mutations on heparin‐induced assembly of tau filaments , 1999, FEBS letters.
[302] Iva Greenwald,et al. Presenilin is required for activity and nuclear access of Notch in Drosophila , 1999, Nature.
[303] D. Selkoe,et al. Two transmembrane aspartates in presenilin-1 required for presenilin endoproteolysis and γ-secretase activity , 1999, Nature.
[304] William J. Ray,et al. A presenilin-1-dependent γ-secretase-like protease mediates release of Notch intracellular domain , 1999, Nature.
[305] E. Kojro,et al. Constitutive and regulated alpha-secretase cleavage of Alzheimer's amyloid precursor protein by a disintegrin metalloprotease. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[306] M. Hutton,et al. Accelerated filament formation from tau protein with specific FTDP‐17 missense mutations , 1999, FEBS letters.
[307] K. Beyreuther,et al. Mechanism of the cleavage specificity of Alzheimer's disease gamma-secretase identified by phenylalanine-scanning mutagenesis of the transmembrane domain of the amyloid precursor protein. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[308] E. Mandelkow,et al. Phosphorylation that detaches tau protein from microtubules (Ser262, Ser214) also protects it against aggregation into Alzheimer paired helical filaments. , 1999, Biochemistry.
[309] John X. Morris,et al. Mutation-specific functional impairments in distinct tau isoforms of hereditary FTDP-17. , 1998, Science.
[310] David C. Lee,et al. An essential role for ectodomain shedding in mammalian development. , 1998, Science.
[311] R. Crowther,et al. Tau Mutations Cause Frontotemporal Dementias , 1998, Neuron.
[312] Joseph D. Buxbaum,et al. Evidence That Tumor Necrosis Factor α Converting Enzyme Is Involved in Regulated α-Secretase Cleavage of the Alzheimer Amyloid Protein Precursor* , 1998, The Journal of Biological Chemistry.
[313] M. Goedert,et al. Tau proteins with FTDP‐17 mutations have a reduced ability to promote microtubule assembly , 1998, FEBS letters.
[314] B. Zlokovic,et al. Human blood-brain barrier receptors for Alzheimer's amyloid-beta 1- 40. Asymmetrical binding, endocytosis, and transcytosis at the apical side of brain microvascular endothelial cell monolayer. , 1998, The Journal of clinical investigation.
[315] Bruce A. Yankner,et al. Aging renders the brain vulnerable to amyloid β-protein neurotoxicity , 1998, Nature Medicine.
[316] A Klug,et al. Mutation in the tau gene in familial multiple system tauopathy with presenile dementia. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[317] Ronald C. Petersen,et al. Association of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17 , 1998, Nature.
[318] G. Schellenberg,et al. Tau is a candidate gene for chromosome 17 frontotemporal dementia , 1998, Annals of neurology.
[319] T. Morgan,et al. Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[320] T. Saido. Alzheimer’s Disease as Proteolytic Disorders: Anabolism and Catabolism of β-Amyloid , 1998, Neurobiology of Aging.
[321] D. Selkoe,et al. Oligomerization of endogenous and synthetic amyloid beta-protein at nanomolar levels in cell culture and stabilization of monomer by Congo red. , 1998, Biochemistry.
[322] Hugo Vanderstichele,et al. Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein , 1998, Nature.
[323] R. Nixon,et al. Increased Neuronal Endocytosis and Protease Delivery to Early Endosomes in Sporadic Alzheimer’s Disease: Neuropathologic Evidence for a Mechanism of Increased β-Amyloidogenesis , 1997, The Journal of Neuroscience.
[324] M. Emmerling,et al. Isolation, chemical characterization, and quantitation of A beta 3-pyroglutamyl peptide from neuritic plaques and vascular amyloid deposits. , 1997, Biochemical and biophysical research communications.
[325] S. Tonegawa,et al. Skeletal and CNS Defects in Presenilin-1-Deficient Mice , 1997, Cell.
[326] D. Price,et al. Presenilin 1 is required for Notch 1 and Dll1 expression in the paraxial mesoderm , 1997, Nature.
[327] Nicole Nelson,et al. A metalloproteinase disintegrin that releases tumour-necrosis factor-α from cells , 1997, Nature.
[328] S. Tsirka,et al. An Extracellular Proteolytic Cascade Promotes Neuronal Degeneration in the Mouse Hippocampus , 1997, The Journal of Neuroscience.
[329] Richard Hollister,et al. Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer's disease , 1997, Annals of neurology.
[330] E. Mandelkow,et al. RNA stimulates aggregation of microtubule‐associated protein tau into Alzheimer‐like paired helical filaments , 1996, FEBS letters.
[331] J. Trojanowski,et al. Full-length amyloid-beta (1-42(43)) and amino-terminally modified and truncated amyloid-beta 42(43) deposit in diffuse plaques. , 1996, The American journal of pathology.
[332] Allan I. Levey,et al. Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo , 1996, Neuron.
[333] J. Hardy,et al. Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1 , 1996, Nature.
[334] R. Crowther,et al. Assembly of microtubule-associated protein tau into Alzheimer-like filaments induced by sulphated glycosaminoglycans , 1996, Nature.
[335] T. Iwatsubo,et al. Amino- and carboxyl-terminal heterogeneity of β-amyloid peptides deposited in human brain , 1996, Neuroscience Letters.
[336] L. Forno,et al. P3 beta-amyloid peptide has a unique and potentially pathogenic immunohistochemical profile in Alzheimer's disease brain. , 1996, The American journal of pathology.
[337] G. Schellenberg,et al. Secreted amyloid β–protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease , 1996, Nature Medicine.
[338] B. Winblad,et al. Predominant deposition of amyloid-beta 42(43) in plaques in cases of Alzheimer's disease and hereditary cerebral hemorrhage associated with mutations in the amyloid precursor protein gene. , 1996, The American journal of pathology.
[339] Sidney Strickland,et al. Excitotoxin-induced neuronal degeneration and seizure are mediated by tissue plasminogen activator , 1995, Nature.
[340] Iva Greenwald,et al. Facilitation of lin-12-mediated signalling by sel-12, a Caenorhabditis elegans S182 Alzheimer's disease gene , 1995, Nature.
[341] J. Rommens,et al. Familial Alzheimer's disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimer's disease type 3 gene , 1995, Nature.
[342] G. Schellenberg,et al. Candidate gene for the chromosome 1 familial Alzheimer's disease locus , 1995, Science.
[343] D. Pollen,et al. Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease , 1995, Nature.
[344] D. Mann,et al. Dominant and differential deposition of distinct β-amyloid peptide species, Aβ N3(pE), in senile plaques , 1995, Neuron.
[345] B. de Strooper,et al. Amyloid precursor protein is not processed by furin, PACE 4, PC1/3, PC2, PC4 and PC5/6 of the furin family of proprotein processing enzymes. , 1995, Biochimica et biophysica acta.
[346] S. Squazzo,et al. Evidence that production and release of amyloid beta-protein involves the endocytic pathway. , 1994, The Journal of biological chemistry.
[347] T. Iwatsubo,et al. Visualization of Aβ42(43) and Aβ40 in senile plaques with end-specific Aβ monoclonals: Evidence that an initially deposited species is Aβ42(43) , 1994, Neuron.
[348] S. Younkin,et al. An increased percentage of long amyloid beta protein secreted by familial amyloid beta protein precursor (beta APP717) mutants. , 1994, Science.
[349] M. Ball,et al. Chemical characterization of A beta 17-42 peptide, a component of diffuse amyloid deposits of Alzheimer disease. , 1994, The Journal of biological chemistry.
[350] D. Selkoe,et al. Cellular processing of β-amyloid precursor protein and the genesis of amyloid β-peptide , 1993, Cell.
[351] P. Lansbury,et al. Seeding “one-dimensional crystallization” of amyloid: A pathogenic mechanism in Alzheimer's disease and scrapie? , 1993, Cell.
[352] M J Ball,et al. Structural alterations in the peptide backbone of beta-amyloid core protein may account for its deposition and stability in Alzheimer's disease. , 1993, The Journal of biological chemistry.
[353] J. Kabat,et al. Molecular characterization of the minimal protease resistant tau unit of the Alzheimer's disease paired helical filament. , 1993, The EMBO journal.
[354] S. Sisodia. Beta-amyloid precursor protein cleavage by a membrane-bound protease. , 1992, Proceedings of the National Academy of Sciences of the United States of America.
[355] Bradley T. Hyman,et al. Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease , 1992, Neurology.
[356] J. Hardy,et al. Early-onset Alzheimer's disease caused by mutations at codon 717 of the β-amyloid precursor protein gene , 1991, Nature.
[357] D. Kirschner,et al. Neurotrophic and neurotoxic effects of amyloid beta protein: reversal by tachykinin neuropeptides. , 1990, Science.
[358] R. Nixon,et al. Enzymatically active lysosomal proteases are associated with amyloid deposits in Alzheimer brain. , 1990, Proceedings of the National Academy of Sciences of the United States of America.
[359] D. Price,et al. Evidence that beta-amyloid protein in Alzheimer's disease is not derived by normal processing. , 1990, Science.
[360] L. Villa-komaroff,et al. Neurotoxicity of a fragment of the amyloid precursor associated with Alzheimer's disease. , 1989, Science.
[361] J. Hardy,et al. The Amyloid Hypothesis of Alzheimer ’ s Disease : Progress and Problems on the Road to Therapeutics , 2009 .
[362] F. Fahrenholz,et al. Effect of a dominant-negative form of ADAM10 in a mouse model of Alzheimer's disease. , 2009, Journal of Alzheimer's disease : JAD.
[363] B. Ghetti,et al. Analysis of tau phosphorylation and truncation in a mouse model of human tauopathy. , 2008, The American journal of pathology.
[364] R. D'Hooge,et al. Lipids revert inert Ab amyloid fibrils to neurotoxic protofibrils that affect learning in mice , 2007 .
[365] T. Klockgether,et al. Nonsteroidal anti-inflammatory drugs repress (cid:1) -secretase gene promoter activity by the activation of PPAR (cid:2) , 2005 .
[366] J. Bonifacino. The GGA proteins: adaptors on the move , 2004, Nature Reviews Molecular Cell Biology.
[367] Rena Li,et al. Amyloid (cid:1) peptide load is correlated with increased (cid:1) -secretase activity in sporadic Alzheimer’s disease patients , 2004 .
[368] P. Wong,et al. Elevated β-secretase expression and enzymatic activity detected in sporadic Alzheimer disease , 2003, Nature Medicine.
[369] N. Seidah,et al. Post-translational processing of b -secretase (BACE) and its ectodomain shedding: the pro- and transmembrane/cytosolic domains affect its cellular activity and amyloid A b production , 2000 .
[370] R. Wang,et al. アミロイド前駆体蛋白質の貫通膜領域のフェニルアラニン‐走査突然変異誘発により確認されたアルツハイマー病γ‐セクレターゼの切断特異性の機序 , 1999 .
[371] C. Harrington,et al. Staging the pathological assembly of truncated tau protein into paired helical filaments in Alzheimer’s disease , 1996, Acta Neuropathologica.