| scholarly article | Q13442814 |
| P2093 | author name string | Toshiharu Suzuki | |
| Ayano Kimura | |||
| Saori Hata | |||
| P2860 | cites work | Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE | Q22010705 |
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| Cleavage of Alzheimer's amyloid precursor protein (APP) by secretases occurs after O-glycosylation of APP in the protein secretory pathway. Identification of intracellular compartments in which APP cleavage occurs without using toxic agents that int | Q74299329 | ||
| A novel substrate for analyzing Alzheimer's disease gamma-secretase | Q77998329 | ||
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| Systematic Aβ Analysis in Drosophila Reveals High Toxicity for the 1-42, 3-42 and 11-42 Peptides, and Emphasizes N- and C-Terminal Residues | Q28546774 | ||
| Identification of a Novel Aspartic Protease (Asp 2) as β-Secretase | Q29042710 | ||
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| Mechanism of intramembrane cleavage of alcadeins by γ-secretase | Q34712076 | ||
| The peculiar role of the A2V mutation in amyloid-β (Aβ) 1-42 molecular assembly | Q35209026 | ||
| ADAMs family members as amyloid precursor protein alpha-secretases | Q35575838 | ||
| Amyloid precursor protein mutation E682K at the alternative β-secretase cleavage β'-site increases Aβ generation | Q36038732 | ||
| BACE overexpression alters the subcellular processing of APP and inhibits Abeta deposition in vivo | Q36321125 | ||
| Overlapping profiles of Aβ peptides in the Alzheimer's disease and pathological aging brains. | Q36424815 | ||
| Inhibiting BACE1 to reverse synaptic dysfunctions in Alzheimer's disease | Q36869427 | ||
| Discrete molecular dynamics study of oligomer formation by N-terminally truncated amyloid β-protein | Q36881483 | ||
| The role of amyloid precursor protein processing by BACE1, the beta-secretase, in Alzheimer disease pathophysiology | Q37225050 | ||
| Intramembrane proteolysis by gamma-secretase | Q37225054 | ||
| Regulation of amyloid beta-protein precursor by phosphorylation and protein interactions | Q37225056 | ||
| A recessive mutation in the APP gene with dominant-negative effect on amyloidogenesis. | Q37309370 | ||
| Alcadein cleavages by amyloid beta-precursor protein (APP) alpha- and gamma-secretases generate small peptides, p3-Alcs, indicating Alzheimer disease-related gamma-secretase dysfunction. | Q37479222 | ||
| γ-Secretase-Dependent Proteolysis of Transmembrane Domain of Amyloid Precursor Protein: Successive Tri- and Tetrapeptide Release in Amyloid β-Protein Production | Q38076426 | ||
| Identification of a beta-secretase activity, which truncates amyloid beta-peptide after its presenilin-dependent generation | Q40684851 | ||
| Glu11 site cleavage and N-terminally truncated A beta production upon BACE overexpression | Q40748378 | ||
| Increased beta-amyloid release and levels of amyloid precursor protein (APP) in fibroblast cell lines from family members with the Swedish Alzheimer's disease APP670/671 mutation. | Q41429343 | ||
| Altered cleavage and secretion of a recombinant beta-APP bearing the Swedish familial Alzheimer's disease mutation | Q41485028 | ||
| Amyloid beta-peptide is produced by cultured cells during normal metabolism | Q41602809 | ||
| The cytoplasmic domain of Alzheimer's amyloid precursor protein is phosphorylated at Thr654, Ser655, and Thr668 in adult rat brain and cultured cells. | Q41941163 | ||
| cDNA isolation of Alzheimer's amyloid precursor protein from cholinergic nerve terminals of the electric organ of the electric ray. | Q42159431 | ||
| Beta-secretase processing in the trans-Golgi network preferentially generates truncated amyloid species that accumulate in Alzheimer's disease brain | Q43888089 | ||
| Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease | Q44132132 | ||
| A basic amino acid in the cytoplasmic domain of Alzheimer's beta-amyloid precursor protein (APP) is essential for cleavage of APP at the alpha-site. | Q47827840 | ||
| Characterization of Abeta11-40/42 peptide deposition in Alzheimer's disease and young Down's syndrome brains: implication of N-terminally truncated Abeta species in the pathogenesis of Alzheimer's disease | Q48463438 | ||
| An electron microscopic study of the development of axons and dendrites by hippocampal neurons in culture. I. Cells which develop without intercellular contacts | Q48638929 | ||
| Expression and localization of X11 family proteins in neurons | Q48692260 | ||
| Metabolic regulation of brain Abeta by neprilysin | Q48869458 | ||
| P433 | issue | 46 | |
| P407 | language of work or name | English | Q1860 |
| P304 | page(s) | 24041-24053 | |
| P577 | publication date | 2016-09-29 | |
| P1433 | published in | Journal of Biological Chemistry | Q867727 |
| P1476 | title | Alternative Selection of β-Site APP-Cleaving Enzyme 1 (BACE1) Cleavage Sites in Amyloid β-Protein Precursor (APP) Harboring Protective and Pathogenic Mutations within the Aβ Sequence | |
| P478 | volume | 291 |
| Q46320596 | APP/Aβ structural diversity and Alzheimer's disease pathogenesis |
| Q64051995 | Aβ34 is a BACE1-derived degradation intermediate associated with amyloid clearance and Alzheimer's disease progression |
| Q47726298 | BACE1 Cleavage Site Selection Critical for Amyloidogenesis and Alzheimer's Pathogenesis. |
| Q90680150 | Emerging Alternative Proteinases in APP Metabolism and Alzheimer's Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP |
| Q45252126 | Entanglement of UPRER in Aging Driven Neurodegenerative Diseases. |
| Q46102764 | Fraction n-Butanol of Radix Notoginseng Protects PC12 Cells from Aβ25-35-Induced Cytotoxicity and Alleviates Cognitive Deficits in SAMP8 Mice by Attenuating Oxidative Stress and Aβ Accumulation. |
| Q41665323 | Modifications and Trafficking of APP in the Pathogenesis of Alzheimer's Disease |
| Q93379781 | Neuroinflammatory Cytokines Induce Amyloid Beta Neurotoxicity through Modulating Amyloid Precursor Protein Levels/Metabolism |
| Q48224032 | New Insights on the Role of Residue 673 of APP in Alzheimer's Disease |
| Q90600056 | Protective effects of BACE1 inhibitory ligand molecules against amyloid beta-induced synaptic and mitochondrial toxicities in Alzheimer's disease |
| Q90463012 | The trans-Golgi network is a major site for α-secretase processing of amyloid precursor protein in primary neurons |
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