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Abeta encodes a cell surface receptor and transmembrane precursor protein that is cleaved by secretases to form a number of peptides. 再加上，我们可以发beta Amyloid 抗体 (277) 和 和数多这个蛋白质的别的产品。
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activation of mTOR (显示 FRAP1 ELISA试剂盒) signalling via RHEB (显示 RHEB ELISA试剂盒) over-expression inhibited the starvation-induced autophagy but did not affect trafficking of tf-Amyloid precursor protein (APP (显示 APP ELISA试剂盒)). These results show tf-APP (显示 APP ELISA试剂盒) can be used to determine how APP (显示 APP ELISA试剂盒) is trafficked through the lysosomal system of the cell.
Study found that FERMT2 (显示 FERMT2 ELISA试剂盒) (a beta3-integrin (显示 ITGB3 ELISA试剂盒) co-activator) was significantly associated with a variation in cerebrospinal fluid Abeta (显示 APP ELISA试剂盒) peptide levels in 2886 Alzheimer's disease cases.Under-expression of FERMT2 (显示 FERMT2 ELISA试剂盒) increases Abeta (显示 APP ELISA试剂盒) peptide production by raising levels of mature APP (显示 APP ELISA试剂盒) at the cell surface and facilitating its recycling
a 99-aa C-terminal fragment of APP (显示 APP ELISA试剂盒),C99, in addition to its localization in endosomes, can also be found in mitochondria-associated endoplasmic reticulum (ER) membranes, where it is normally processed rapidly by gamma-secretase.
Photoinduced electrons of g-C3 N4 generate reactive oxygen resulting in photooxidation of amyloid peptides that blocks Abeta (显示 APP ELISA试剂盒) aggregation.
Studies indicate that amyloid precursor-like protein 2 (APLP2 (显示 APLP2 ELISA试剂盒)) and amyloid precursor protein (APP (显示 APP ELISA试剂盒)) are linked to increased tumor cell proliferation, migration, and invasion.
the precise and complex regulation of APP (显示 APP ELISA试剂盒) phosphorylation, abundance, and cleavage impacts the generation of nuclear spheres, which are under discussion of being of relevance in neurodegeneration and dementia.
Decreased lipoprotein endocytosis and transcytosis of APP (显示 APP ELISA试剂盒) to the axon suggest that a neuron-specific impairment in endocytic axonal delivery of lipoproteins and other key materials might compromise synaptic maintenance in familial Alzheimer's disease.
Our results suggested that hAPP was more likely an important factor inhibiting adult neurogenesis, and Abeta (显示 APP ELISA试剂盒) was not the major factor affecting neurogenesis in the adult hippocampus of hAPP mice.
the AOEP2 peptide binds to Abeta (显示 APP ELISA试剂盒) monomers and inhibits the formation of Abeta (显示 APP ELISA试剂盒) oligomers and beta-sheet structure, reduces Abeta42-induced neurotoxicity, and decreases the release of proinflammatory cytokines.
BECN1 (显示 BECN1 ELISA试剂盒)-APP (显示 APP ELISA试剂盒) association and BECN1 (显示 BECN1 ELISA试剂盒)-dependent APP (显示 APP ELISA试剂盒) endocytosis and degradative trafficking were negatively regulated by active AKT (显示 AKT1 ELISA试剂盒).
The authors concluded that the FcgammaRIIb-SHIP2 (显示 INPPL1 ELISA试剂盒) axis links Abeta (显示 APP ELISA试剂盒) neurotoxicity to tau pathology by dysregulating phosphoinositide metabolism, providing insight into therapeutic potential against Alzheimer's disease.
results suggest that PrP(C (显示 PRNP ELISA试剂盒)) recognizes structural features common to both Abeta (显示 APP ELISA试剂盒) oligomers and fibril ends and that this interaction could contribute to the neurotoxic effect of Abeta (显示 APP ELISA试剂盒) aggregates.
Our study provides the first direct evidence that Abeta, an AD-linked factor, is associated to the pathogenesis of ALS and provides molecular clues to understand common aggregation mechanisms in the pathogenesis of neurodegenerative diseases.
Although hyperactivity and hypersynchronicity were respectively detected in mice expressing the PS2 (显示 PDCD6 ELISA试剂盒)-N141I or the APP (显示 APP ELISA试剂盒) Swedish mutant alone, the increase in cross-frequency coupling specifically characterized the 6-month-old PS2APP mice, just before the surge of the cognitive decline
these results uncover a novel role for mDia1 in Abeta-mediated synaptotoxicity and demonstrate that inhibition of MT dynamics and accumulation of PTMs are driving factors for the induction of tau-mediated neuronal damage.
APP (显示 APP ELISA试剂盒) and its metabolites are capable of influencing the basic physiology of the pancreas.
treatment of APP/E4/Abca1+/- mice with liver X receptor (LXR) agonist T0 ameliorates APOE4-induced Alzheimer's disease (AD)-like pathology and therefore targeting the LXR-ABCA1-APOE regulatory axis could be effective as a potential therapeutic approach in AD patients, carriers of APOEepsilon4
These results provide evidence supporting a key role for the p38 MAPK (显示 MAPK14 ELISA试剂盒) signaling pathway which is involved in the regulation of Abeta1-42 internalization in the parietal cortex and hippocampus of mouse through LRP1 (显示 LRP1 ELISA试剂盒) in vivo.
increased APP (显示 APP ELISA试剂盒) and/or beta-CTF (显示 NFIA ELISA试剂盒) impact the endocytic pathway to disrupt NGF (显示 NGFB ELISA试剂盒) trafficking and signaling, resulting in trophic deficits in basal forebrain cholinergic neurons.
This gene encodes a cell surface receptor and transmembrane precursor protein that is cleaved by secretases to form a number of peptides. Some of these peptides are secreted and can bind to the acetyltransferase complex APBB1/TIP60 to promote transcriptional activation, while others form the protein basis of the amyloid plaques found in the brains of patients with Alzheimer disease. Mutations in this gene have been implicated in autosomal dominant Alzheimer disease and cerebroarterial amyloidosis (cerebral amyloid angiopathy). Multiple transcript variants encoding several different isoforms have been found for this gene.
alzheimer disease amyloid protein
, amyloid beta A4 protein
, beta-amyloid peptide
, cerebral vascular amyloid peptide
, peptidase nexin-II
, protease nexin-II
, amyloid beta (A4) precursor protein (peptidase nexin-2, Alzheimer disease)
, amyloid beta (A4) precursor protein (protease nexin-II, Alzheimer disease)
, beta-amyloid precursor protein
, alzheimer disease amyloid A4 protein homolog
, amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease)
, amyloid A4
, amyloidogenic glycoprotein
, protease nexin II