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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. Additionally we are shipping beta Amyloid Antibodies (262) and beta Amyloid Proteins (3) and many more products for this protein.
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Amyloid precursor protein (APP (show APP ELISA Kits)) 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 (show APP ELISA Kits) 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 (show APP ELISA Kits) 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 (show APP ELISA Kits) accumulation with chronic less sleep.
This review highlights the existing link between oxidative stress and Alzheimer's disease, and the consequences towards the ABETA (show APP ELISA Kits) peptide and surrounding molecules in terms of oxidative damage. [review]
overall results and observations regarding human serum albumin (show ALB ELISA Kits), amyloid-beta, and metal ions advance our knowledge of how protein-protein interactions associated with amyloid-beta and metal ions could be linked to Alzheimer's disease pathogenesis
electrostatic interactions in the center of the Abeta (show APP ELISA Kits) peptide sequence play a crucial role in the three-dimensional fold of the fibrils, and by inference, fibril-induced neuronal toxicity and AD pathogenesis
This study applies methodologies on the initial stages of aggregation of a hexamer of Alzheimer's amyloid beta fragment 25-35 (ABETA (show APP ELISA Kits) 25-35) and finds that transitions within the hexameric aggregate are dominated by entropic barriers and speculates that especially the conformation entropy plays a major role in the formation of the fibril as a rate limiting factor.
c-Abl is activated in AbetaOs exposed neurons and in Alzheimer's disease patient's brain, and the inhibition of activated c-Abl ameliorates cognitive deficits
Inflammasome-derived cytokine IL18 (show IL18 ELISA Kits) suppresses amyloid-induced seizures in Alzheimer-prone mice.
pharmacological inhibition of PARP-1 (show PARP1 ELISA Kits) reversed both particulate matter-induced Abeta (show APP ELISA Kits) increase and glial activation.
The concentrations of Abeta (show APP ELISA Kits) (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 (show APP ELISA Kits) (1-42) in mice with later stage AD, reduced astrocyte staining was observed compared with WT mice.
work expands the current knowledge regarding Abeta (show APP ELISA Kits) seeding and the consequences thereof and attributes microglia an important role in diminishing Abeta (show APP ELISA Kits) seeding by environmental enrichment.
This study demonstrated that APP (show APP ELISA Kits) 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 (show APP ELISA Kits) in the brain, consistent with a causal effect. Increased nuclear translocation of histone deacetylase 4 (HDAC4 (show HDAC5 ELISA Kits)) 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 (show APP ELISA Kits) 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.
Therefore, APP (show APP ELISA Kits) modulates Nav1.6 (show SCN8A ELISA Kits) sodium channels through a Go-coupled JNK (show MAPK8 ELISA Kits) pathway, which is dependent on phosphorylation of APP (show APP ELISA Kits) at Thr668.
These findings suggest that in the absence of CLU (show CLU ELISA Kits), Abeta (show APP ELISA Kits) clearance shifts to perivascular drainage pathways, resulting in fewer parenchymal plaques but more CAA because of loss of CLU (show CLU ELISA Kits) chaperone activity, complicating the potential therapeutic targeting of CLU (show CLU ELISA Kits) for AD.
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