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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 (261) et beta Amyloid Protéines (3) et beaucoup plus de produits pour cette protéine.
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Data show that phospholipase D3 (PLD3) functions in endosomal protein sorting and plays an important role in regulating amyloid precursor protein (APP (Montrer APP Kits ELISA)) processing.
Data show that amyloid precursor protein (APP (Montrer APP Kits ELISA)) dimerization affects its interaction with LDL receptor (Montrer LDLR Kits ELISA) related protein 1 (LRP1 (Montrer LRP1 Kits ELISA)) and LDL-receptor (Montrer LDLR Kits ELISA) related protein SorLA (SorLA (Montrer SORL1 Kits ELISA)), suggesting that APP (Montrer APP Kits ELISA) dimerization modulates its interplay with sorting molecules and in turn its localization and processing.
overexpression of APP (Montrer APP Kits ELISA) may promote the onset of seborrhoeic keratosis and is a marker of skin ageing and UV damage.
Structural and biochemical differences between the Notch (Montrer NOTCH1 Kits ELISA) and the amyloid precursor protein (Montrer APP Kits ELISA) transmembrane domains.
Gnetin C may thereby prevent Abeta (Montrer APP Kits ELISA) toxicity by suppressing BACE1 (Montrer BACE Kits ELISA) and enhancing MMP-14 (Montrer MMP14 Kits ELISA), together with reducing both internalization and oligomerization of exogenous Abeta (Montrer APP Kits ELISA) monomers.
Amyloid precursor protein (APP (Montrer APP Kits ELISA)) binds the HIV-1 Gag polyprotein, retains it in lipid rafts and blocks HIV-1 virion production and spread.
ABETA(1-42) doses >5 microM (Montrer APP Kits ELISA) inhibited the growth of U87 cells compared with the 0 microM group after 24 and 48 h treatment.
The mechanism involved in the interaction of HSP60-Ass conjugate with HLA-DR-DRB allele considering the fact that Ass (1-42) is highly immunogenic in human and interactions evoked highly robust T-cell response through MHC class II binding predictions.
Abeta (Montrer APP Kits ELISA) fibrils start to accumulate predominantly within certain parts of the default mode network in preclinical Alzheimer's disease and already then affect brain connectivity.
findings show adverse effects of one-night sleep deprivation on brain ABB and expand on prior findings of higher Abeta (Montrer APP Kits ELISA) accumulation with chronic less sleep.
These results support the proposition that Aβ release during thrombosis serves as part of a natural defense against infection.
These data suggest a novel regulatory function of juxta- and intra-membrane domains on the metabolism and function of APP (Montrer APP Kits ELISA).
Inflammasome-derived cytokine IL18 (Montrer IL18 Kits ELISA) suppresses amyloid-induced seizures in Alzheimer-prone mice.
pharmacological inhibition of PARP-1 (Montrer PARP1 Kits ELISA) reversed both particulate matter-induced Abeta (Montrer APP Kits ELISA) increase and glial activation.
The concentrations of Abeta (Montrer APP Kits ELISA) (1-42) were also significantly higher in early stage Alzheimer's disease (AD) mice compared with WT mice, however, the levels were markedly lower compared with later stage AD mice, as determined by ELISA. In addition to increased levels of Abeta (Montrer APP Kits ELISA) (1-42) in mice with later stage AD, reduced astrocyte staining was observed compared with WT mice.
work expands the current knowledge regarding Abeta (Montrer APP Kits ELISA) seeding and the consequences thereof and attributes microglia an important role in diminishing Abeta (Montrer APP Kits ELISA) seeding by environmental enrichment.
This study demonstrated that APP (Montrer APP Kits ELISA) as a novel receptor for Slit ligand mediating axon guidance and neural circuit formation.
In vivo, the NHE6 knockout (NHE6(KO)) mouse model showed elevated Abeta (Montrer APP Kits ELISA) in the brain, consistent with a causal effect. Increased nuclear translocation of histone deacetylase 4 (HDAC4 (Montrer HDAC5 Kits ELISA)) in ApoE4 astrocytes, compared with the nonpathogenic ApoE3 allele, suggested a mechanistic basis for transcriptional down-regulation of NHE6.
This commentary reviews the role of the Alzheimer amyloid peptide Abeta (Montrer APP Kits ELISA) on basal synaptic transmission, synaptic short-term plasticity, as well as short- and long-term potentiation in transgenic mice, with a special focus on N-terminal truncated Abeta4-42.
ADAP KO mice developed glomerular pathology. ADAP KO podocytes lack cell protrusions with actin cytoskeleton forming circumferential stress fibers.
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