| protein
| gamma secretase putatively (PSEN1 and PSEN2) to cleavage of APP in Abeta 42 with deposition in brain (fibrillar myeloid plaques to cause neurodegeneration) |
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APBB1, via its C-ter region (LRP2 interacts with APP and APBB1 in neurons  |
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sortilin-related receptor, L(DLR class) A repeats-containing (SORL1) |
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APP and APLP bind to heme oxygenase (HO) and inhibit HO activity |
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amyloid beta (A4) precursor protein-binding, family B, member 1 (Fe65) |
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forms a multimeric complex with the nuclear adaptor protein Fe65 and the histone acetyltransferase Tip60 |
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amyloid beta (A4) precursor protein-binding, family A, member 1 (APBA1) |
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amyloid beta (A4) precursor protein-binding, family A, member 2 (ABPA2) |
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amyloid beta (A4) precursor protein-binding, family A, member 3 (APBA3) |
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amyloid beta (A4) precursor protein-binding, family B, member 2 (APBB2) |
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amyloid beta (A4) precursor protein-binding, family B, member 3 (APBB3) |
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acetylcholinesterase (AChE) |
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protein interacting with APP tail 1 (PAT1) |
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heparan sulfate proteoglycan 2 (HSPG2) |
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Human bleomycin hydrolase (hBH) |
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Disruption of the disabled-1 gene (Dab1) |
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fibulin 1 (FBLN1) |
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Calreticulin (CALR) |
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glyceraldehyde-3-phosphate dehydrogenase (GAPDH) |
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growth factor receptor-bound protein 2 (GRB2) |
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SHC (Src homology 2 domain containing) transforming protein 1 (SHC1) |
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gelsolin (GSN) |
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intracellular amyloid beta-peptide (A beta) binding protein (ERAB) |
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kinesin-I |
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kininogen 1 (KING1) |
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low density lipoprotein (LDL) receptor-related protein 1B (LRP1B) |
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Jun NH2-terminal kinase (JNK) interacting protein 1 (JIP1) |
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59-kDa APP-binding protein, called APP-BP1 |
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nicastrin (NCSTN) |
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Notch inhibitors Numb and Numb-like in mouse brain |
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alpha 1-antichymotrypsin (ACT) |
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synuclein, alpha (non A4 component of amyloid precursor) (SNCA) |
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spondin 1, extracellular matrix protein (SPON1) |
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Transforming growth factor-beta (TGF-beta) |
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TM2 domain containing 1 (TM2D1) |
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mitogen-activated protein kinase 8 interacting protein 1 (MAPK8IP1 aslo known as JIP-1) |
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presenilin 1 (PS1) and presenilin 2 (PS2) |
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human serine protease HtrA2/Omi |
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death receptor 6 (DR6) |
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alpha7 nicotinic acetylcholine receptor (alpha7nAChR) |
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cell death mediator p75(NTR) |
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microtubule-associated protein tau (MAPT) |
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have major interactions with ferroportin to facilitate iron export from certain cells including neurons |
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NSG1 profoundly affects the processing of APP production |
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GAS1 negatively regulated APP intracellular trafficking |
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GULP1-APP interaction is mediated by the NPTY motif of APP and the GULP1 PTB (phosphotyrosine-binding) domain ( |
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CDH2 expression facilitates cis-dimerization of APP ( |
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interaction between APP and neuroligin-1 (NLGN1), increasing the formation of APP oligomers, and suggesting that this interaction could triggers the targeting of APP oligomer to the postsynaptic regions of excitatory synapses |
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mechanistic link between APOE-regulated cholesterol homeostasis and APP degradation |
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HAP1 regulates APP subcellular trafficking to the non-amyloidogenic pathway and may negatively regulate APP production in neurons |
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APP-activated NFATC3 proteins were associated with astrocytic BACE1 gene expression via direct interaction with the BACE1 promoter region |
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UBQLN1 inhibits the maturation of APP by sequestering it in the early secretory pathway, primarily within the Golgi apparatus |
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APP endocytic trafficking to lysosomes for degradation is a major APP clearance pathway that is differentially regulated by APOE isoforms |
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APBB1 might have signalling properties together with APP and LRP1 |
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APOE influences soluble APP metabolism not through direct binding to soluble APP in solution but through its actions with other interacting receptors/transporters and cell surfaces |
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is able to affect the downstream effects of protease inhibition in neural cells including enhancement of CTSB activity, with these changes in CTSB significantly and inversely related to the levels of ubiquitinated protein |
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interacts with MAP1LC3B via OPTN/optineurin and is degraded by an autophagic process mediated by the PRKAA1 pathway |
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APP-stimulated neuronal differentiation of neural stem/progenitor cells (NSPCs) is mediated by NEUROG2 |
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APP enhances SCN8A sodium channel cell surface expression through a Go-coupled JNK pathway |
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WASF1 interacts and colocalizes with APP in the Golgi apparatus |
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APP,is a novel interaction partner of PIKFYVE (furthermore, it has been shown that APP modulates PIKFYVE function and PI(3,5)P2 dynamics) |
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SEPTIN8 modulates likely bta-amyloidogenic processing of APP through a mechanism affecting the intracellular sorting and accumulation of BACE1 |
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EGR1 promotes APP synthesis via transcriptional activation of BACE1, suggesting that EGR1 plays role in activation of BACE1 and acceleration of APP synthesis in Alzheimer disease brain |
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GKN1 directly interacted with APP C-terminal fragments, C83 and C99 |
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novel role for SORL1 as a physiological and pathological EPHA4 modulator, which attenuates synaptotoxic EPHA4 activation and cognitive impairment associated with APP-induced neurodegeneration in Alzheimer disease |
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| transgenic mouse models expressing human Alzheimer's A beta peptide exhibit brain regions severely affected in Alzheimer's disease resulting in extensive neuronal degeneration (LaFerla 1995) | |
double mutant (tau/APP) mice exhibited neurofibrillary tangle pathology substantially enhanced in the limbic system and olfactory cortex (Lewis 2001) |
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co-expression of both mutant transgenes presenilin 1 and APP results in acceleration of amyloid accumulation and associative learning deficits (Dineley 2002) |
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expression of human Abeta42 peptide in the Drosophila brain led to the formation of diffused amyloid deposits, age-dependent learning defects, and extensive neurodegeneration and Abeta40 caused only age-dependent learning defects (Iijima 2004) |
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FVB/N mice overexpressing human APP695 develop a central nervous system disorder and die prematurely, precluding development of Abeta peptide amyloid plaques whereas 129S6 mice are resistant to the lethal effects of APP overexpression (Krezowski 2004) |
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gene expression analysis revealed that the genes related to mitochondrial energy metabolism and apoptosis were up-regulated in 2-month-old Tg2576 mouse AD model and that the same genes were up-regulated at 5 and 18 months of age suggesting that mitochondrial energy metabolism is impaired by the expression of mutant APP and/or Abeta, and that the up-regulation of mitochondrial genes is a compensatory response (Reddy 2004) |
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estrogen-deficient APP23 mice exhibited greatly reduced brain estrogen, early-onset and increased beta amyloid peptide (Abeta) deposition and increased Abeta production (Yue 2005) |
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memory deficits in middle-aged Tg2576 mice are caused by the extracellular accumulation of a 56-kDa soluble amyloid-beta assembly suggesting that Abeta*56 impairs memory independently of plaques or neuronal loss, and may contribute to cognitive deficits associated with Alzheimer's disease (Lesné 2006) |
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Lack of NO synthase 2 in the amyloid precursor protein Swedish mutant mouse increased insoluble beta-amyloid peptide levels, neuronal degeneration, caspase-3 activation, and tau cleavage (Colton 2006) |
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Alzheimer disease mice deficient in Ccr2 accumulated Abeta earlier and died prematurely. Ccr2 deficiency accelerates early disease progression and markedly impairs microglial accumulation (El Khoury 2007) |
