Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
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 (270) and and many more products for this protein.
Showing 1 out of 2 products:
These results confirm the involvement of amyloid precursor protein (APP (show APP ELISA Kits)) in synaptogenesis and provide evidence to suggest that human APP (show APP ELISA Kits) overexpression specifically disturbs the structural and functional organization of active zone and results in altered Bruchpilot distribution and lowered probability of spontaneous neurotransmitter release.
Study showed that the APP (show APP ELISA Kits) Osaka mutation has dual effects: it causes a loss-of-function of APP (show APP ELISA Kits) and gain-of-toxic-function of Abeta (show APP ELISA Kits), though the latter seems to come out only after the former causes GABAergic depletion. Also present OSK-KI mice as a mouse model to replicate the hereditary form of recessive familial Alzheimer's disease.
results suggest that co-oligomers are a common form of aggregate when Abeta (show APP ELISA Kits) isoforms are present in solution and may potentially play a significant role in Alzheimer's disease.
This study reports the transition dipole strengths and frequencies of the amyloid beta-sheet amide I mode for the aggregated proteins amyloid-beta1-40, calcitonin (show CALCA ELISA Kits), alpha-synuclein, and glucagon (show GCG ELISA Kits).
Overall, these findings suggest that the ability of apoE (show APOE ELISA Kits) fragments to promote Abeta42 intraneuronal accumulation is specific for both the apoE4 isoform and the particular structural and thermodynamic properties of the fragment.
This study structurally characterized ABETA (show APP ELISA Kits) 40 and ABETA (show APP ELISA Kits) 42 monomers through pentamers which were converted from previously derived coarse-grained (DMD4B-HYDRA) simulations into all-atom conformations and subjected to explicit-solvent Molecular Dynamics.
Shape complementarity between close-packed residues plays a critical role in the amyloid aggregation process. This study probes such "steric zipper" interactions in amyloid-beta (ABETA (show APP ELISA Kits) 40), whose aggregation is linked to Alzheimer's disease, by replacing natural residues by their stereoisomers. Stereoisomers can cause complex site dependent changes in amyloid properties.
Besides, the promoting effect of Zn2+ on ABETA42 fast aggregation peaked at pH 6.8-7.8, which includes the pH values of the cerebrospinal fluid (pH 7.3) and hippocampus (pH 7.15-7.35). The findings demonstrate the significant effect of Zn2+ on ABETA (show APP ELISA Kits) aggregation and provide new insight into its mechanisms.
Taken together, these results suggest that ApoE4 enhances Abeta (show APP ELISA Kits) inhibition of insulin (show INS ELISA Kits)-stimulated AMPA (show GRIA3 ELISA Kits) receptor function, which accelerates memory impairment in ApoE4xAPP mice.
The authors found that as already shown for oligomeric Abeta (show APP ELISA Kits), also oligomeric Tau can bind to amyloid precursor protein (APP (show APP ELISA Kits)). Moreover, efficient intra-neuronal uptake of oligomeric Abeta (show APP ELISA Kits) and oligomeric Tau requires expression of APP (show APP ELISA Kits).
Results show that the duration of UP state, which is a key feature of cortical synaptic integration occurring predominantly during slow-wave sleep, is significantly increased in the prefrontal cortex in the absence of APP (show APP ELISA Kits). This was accompanied by a specific reduction in the glutamine synthetase (show GLUL ELISA Kits) and tissue GABA content and sequential upregulation in the levels of GABA-B receptor expression.
results support the hypothesis that the miR (show MLXIP ELISA Kits)-132/212 network, including Sirt1 (show SIRT1 ELISA Kits) and likely other target genes, contributes to abnormal Abeta (show APP ELISA Kits) metabolism and senile plaque deposition in AD.
Activation of CaMKIV (show CAMK4 ELISA Kits) by soluble amyloid-beta1-42 impedes trafficking of axonal vesicles and impairs activity-dependent synaptogenesis
Abpp (show APP ELISA Kits) /KPI(R13I) mutant mice were similarly deficient as Abpp (show APP ELISA Kits) knock out mice in regulating cerebral thrombosis in experimental models of carotid artery thrombosis and intracerebral hemorrhage.
The cognitive function of APP (show APP ELISA Kits)/PS1 (show PSEN1 ELISA Kits) 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 (show APP ELISA Kits) heterozygosity results in greater decreases of cortical APP (show APP ELISA Kits) in Transgenic (Tg) versus non-Tg mice. Mutant huntingtin (show HTT ELISA Kits) transgenic mice develop brain iron accumulation as a result of greater suppression of APP (show APP ELISA Kits) 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.
Mass spectrometry analysis of APP (show APP ELISA Kits) intracellular domains revealed differential processing of APP (show APP ELISA Kits)-C83, APP (show APP ELISA Kits)-C89, and APP (show APP ELISA Kits)-C99 by gamma-secretase already at the epsilon-cleavage stage. This mechanistic insight could aid in developing substrate-targeted modulators of APP (show APP ELISA Kits)-C99 processing to specifically lower the Abeta42:Abeta40 ratio without compromising gamma-secretase function.
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.
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 (show APP ELISA Kits).
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