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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. De plus, nous expédions beta Amyloid Anticorps (274) et et beaucoup plus de produits pour cette protéine.
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Taken together, these results suggest that ApoE4 enhances Abeta (Montrer APP Kits ELISA) inhibition of insulin (Montrer INS Kits ELISA)-stimulated AMPA (Montrer GRIA3 Kits ELISA) receptor function, which accelerates memory impairment in ApoE4xAPP mice.
The authors found that as already shown for oligomeric Abeta (Montrer APP Kits ELISA), also oligomeric Tau can bind to amyloid precursor protein (APP (Montrer APP Kits ELISA)). Moreover, efficient intra-neuronal uptake of oligomeric Abeta (Montrer APP Kits ELISA) and oligomeric Tau requires expression of APP (Montrer APP Kits ELISA).
Reco (Montrer APP Kits ELISA)mbinant mutant KPI(R13I) domain of ABPP was ineffective (Montrer APP Kits ELISA)in the inhibition of pro-thrombotic proteinases and did not inhibit the clotting of plasma in vitro.
Analysis of biochemical fractions of Alzheimer's disease brain extract indicate that the seeding-activity correlated with the presence of ABETA (Montrer APP Kits ELISA) peptide and ABETA (Montrer APP Kits ELISA)-derived aggregates. In vitro-formed fibrils were also active but their activity was low and depending on the fibril structure and conditions of fibril formation.
A comprehensive understanding of the still undefined contribution of Abeta (Montrer APP Kits ELISA) truncations to the disease pathogenesis and their potential as novel therapeutic targets.
The amyloid hypothesis proposes that Alzheimer's Disease is caused by altered beta-amyloid precursor protein expression or APP (Montrer APP Kits ELISA)-mutation-induced Ab aggregation, following an imbalance between Ab production and Ab clearance.
Phosphorylation of amyloid precursor protein by mutant LRRK2 promotes AICD activity and neurotoxicity in Parkinson's disease.
Mass spectrometry analysis of APP (Montrer APP Kits ELISA) intracellular domains revealed differential processing of APP (Montrer APP Kits ELISA)-C83, APP (Montrer APP Kits ELISA)-C89, and APP (Montrer APP Kits ELISA)-C99 by gamma-secretase already at the epsilon-cleavage stage. This mechanistic insight could aid in developing substrate-targeted modulators of APP (Montrer APP Kits ELISA)-C99 processing to specifically lower the Abeta42:Abeta40 ratio without compromising gamma-secretase function.
enzymes known to act in other metabolic pathways, such as meprin beta (Montrer MEP1B Kits ELISA), have been found to cleave APP (Montrer APP Kits ELISA) to yield products known to participate in AD pathologies. This review provides an overview of current knowledge of conventional and novel APP (Montrer APP Kits ELISA) processing.
study provides molecular insights into the design of amyloidogenic inhibitors to cure various neurodegenerative and amyloid-associated diseases, as NABi would regulate aggregation of other toxic beta-sheet proteins other than Abeta (Montrer APP Kits ELISA).
Activation of CaMKIV (Montrer CAMK4 Kits ELISA) by soluble amyloid-beta1-42 impedes trafficking of axonal vesicles and impairs activity-dependent synaptogenesis
Abpp (Montrer APP Kits ELISA) /KPI(R13I) mutant mice were similarly deficient as Abpp (Montrer APP Kits ELISA) knock out mice in regulating cerebral thrombosis in experimental models of carotid artery thrombosis and intracerebral hemorrhage.
The cognitive function of APP (Montrer APP Kits ELISA)/PS1 (Montrer PSEN1 Kits ELISA) mice was impaired at 10months of age; moreover, the hypermetabolic state identified in various brain regions at 5months of age was also significantly decreased.
APP (Montrer APP Kits ELISA) heterozygosity results in greater decreases of cortical APP (Montrer APP Kits ELISA) in Transgenic (Tg) versus non-Tg mice. Mutant huntingtin (Montrer HTT Kits ELISA) transgenic mice develop brain iron accumulation as a result of greater suppression of APP (Montrer APP Kits ELISA) levels. Elevated brain iron in Tg mice was associated with a decline in motor endurance consistent with a disease promoting effect of iron in the YAC128 model of human Huntington's Disease.
Data show that exosomal amyloid precursor protein C-terminal fragments (APP-CTFs) and bis(monoacylglycero)phosphate (BMP) as candidate biomarkers diagnostic of endolysosomal dysfunction associated with neurodegenerative disorders.
Conducted in vivo extracellular recording to investigate cholinergic compound action potentials of the superior cervical ganglion (SCG) in APP (Montrer APP Kits ELISA)(-/-) and littermate wild-type (WT) mice; found that APP (Montrer APP Kits ELISA) not only regulates presynaptic activity, but also affects postsynaptic function at cholinergic synapses in SCG; also alpha4beta2 and alpha7 nicotinic acetylcholine receptors are reduced in the absence of APP (Montrer APP Kits ELISA).
App (Montrer APP Kits ELISA)-KI mouse lines with different levels of pathophysiology are useful models of AD.
Loss of Abpp (Montrer APP Kits ELISA) is associated with cognitive impairment.
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