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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 (277) and beta Amyloid Proteins (3) and many more products for this protein.
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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
RelA (show NFkBP65 ELISA Kits), RelB (show RELB ELISA Kits) and c-Rel (show NFkBP65 ELISA Kits) can be activated by Abeta1-40, all of which mediate pro-inflammatory cytokine transcription and retinal pigment epithelium damage.
specific balance between the concentrations of monomeric and fibrillar alpha-synuclein determines the outcome of the Abeta42 aggregation reaction
Nuclear HSP70 (show HSP70 ELISA Kits) leads to enhancement of vaccinia H1-related phosphatase (VHR (show DUSP3 ELISA Kits)) activity via protein-protein interaction rather than its molecular chaperone (show HSP90AA1 ELISA Kits) activity, thereby suppressing excessive ERK (show EPHB2 ELISA Kits) activation. Downregulation of either VRK3 or HSP70 (show HSP70 ELISA Kits) rendered cells vulnerable to glutamate (show GRIN1 ELISA Kits)-induced apoptosis.
The authors show that lipoproteins including brain (apoE (show APOE ELISA Kits)) and circulating (high-density lipoprotein, HDL (show HSD11B1 ELISA Kits)) synergize to facilitate beta-amyloid transport across bioengineered human cerebral vessels.
The Network analyses identified APP (show APP ELISA Kits) expression in temporal cortex in patient with late-onset Alzheimer's disease.
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.
Chronic Dyrk1 (show DYRK1A ELISA Kits) inhibition reversed cognitive deficits in Alzheimer's disease transgenic mice via reduction of APP (show APP ELISA Kits) and phosphorylated tau pathology.
The results of the present study substantiate that cGMP has a role in the endocytic pathway of APP (show APP ELISA Kits) and suggest a scenario where the cyclic nucleotide enhances the production of Abeta (show APP ELISA Kits) by favoring the trafficking of APP (show APP ELISA Kits) from the cell cortex to the endolysosomal compartment.
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 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.
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