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Cerebral deposition of amyloid beta peptide is an early and critical feature of Alzheimer's disease. Additionally we are shipping beta-Site APP-Cleaving Enzyme 1 Antibodies (269) and beta-Site APP-Cleaving Enzyme 1 Proteins (31) and many more products for this protein.
Showing 10 out of 62 products:
Lee, Park, Han: Effect of mycelial extract of Clavicorona pyxidata on the production of amyloid beta-peptide and the inhibition of endogenous beta-secretase activity in vitro. in Journal of microbiology (Seoul, Korea) 2007
Show all 3 Pubmed References
Human BACE ELISA Kit for Sandwich ELISA - ABIN1110850
Johnson, Drugan, Miller, Evans: 38 in 1991
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Human BACE ELISA Kit for Sandwich ELISA - ABIN365021
Qian, Ding, Cheng, Zhu, Zhao, Jin, Guan, Zhang, Chen, Xu: Early biomarkers for post-stroke cognitive impairment. in Journal of neurology 2012
Mouse (Murine) BACE ELISA Kit for Sandwich ELISA - ABIN424458
Che, Zhou, Zhang, Zhang, Ding, Yanagita, Xu, Xue, Wang: Comparative study of the effects of phosphatidylcholine rich in DHA and EPA on Alzheimer's disease and the possible mechanisms in CHO-APP/PS1 cells and SAMP8 mice. in Food & function 2017
This study shown that the protein expression of BACE1 is downregulated by chronic treatment with donepezil. This effect may be interpreted as evidence of disease modification.
Endosome-to-TGN (show TG ELISA Kits) trafficking of BACE1 is regulated by Par3 (show F2RL2 ELISA Kits) and aPKC. This is a mechanism in pathogenesis of Alzheimer disease.
Results indicate that SNX4-mediated regulation of the steady-state levels and trafficking of BACE1, as well as the subsequent increase in BACE1-mediated cleavage, may be relevant to Alzheimer's disease progression.
We discuss how the underlying mechanisms can be conceived and develop scenarios how the regulation of ion conductances by BACE1 might shape electric activity in the intact and diseased brain and heart
Study showed that serum deprivation enhances ADAM10 (show ADAM10 ELISA Kits)/17-mediated cleavage and secretion of enzymatically active BACE1. This could be the result of alterations in the lipid composition of the membrane that lead in disruption of membrane compartmentalization in lipid rafts and non-lipid rafts. At present the significance of BACE1 shedding in the development of Alzheimer's disease is unclear.
Data suggest that trimerization of BACE1 requires transmembrane sequences (TMSs) and cytoplasmic domains, with residues Ala463 and Cys466 buried within trimer interface of the sulfur-rich core of TMSs; BACE1 appears to play role in compartmentalization of intracellular copper by transferring cytosolic copper to intracellular compartments.
SEPT8 (show SEPT8 ELISA Kits) modulates beta-amyloidogenic processing of APP (show APP ELISA Kits) through a mechanism affecting the intracellular sorting and accumulation of BACE1.
the depletion of BIN1 (show BIN1 ELISA Kits) increases cellular BACE1 levels through impaired endosomal trafficking and reduces BACE1 lysosomal degradation, resulting in increased Ab production. Our findings provide a mechanistic role of BIN1 (show BIN1 ELISA Kits) in the pathogenesis of Alzheimer disease (AD), as a novel genetic regulator of BACE1 levels and Ab production
in vitro BACE1-activity assays demonstrate that palmitoylation-dependent dimerization of APP (show APP ELISA Kits) promotes beta-cleavage of APP (show APP ELISA Kits) in lipid-rich detergent resistant cell membranes (DRMs), when compared to total APP (show APP ELISA Kits).
The circular RNA ciRS-7 promotes APP (show APP ELISA Kits) and BACE1 degradation in an NF-kappaB (show NFKB1 ELISA Kits)-dependent manner.
We aimed to explore the potential therapeutic effect of PGC-1alpha (show PPARGC1A ELISA Kits) by generating a lentiviral vector to express human PGC-1alpha (show PPARGC1A ELISA Kits) and target it by stereotaxic delivery to hippocampus and cortex of APP23 transgenic mice . Four months after hPGC-1alpha injection, mice showed improved spatial and recognition memory concomitant with a significant reduction in Abeta (show APP ELISA Kits) deposition, associated with a decrease in BACE1 expression
that BACE1 deficiency enhances proliferation of Schwann cell due to the elevated Jag1 (show JAG1 ELISA Kits)/Delta1-Notch (show NOTCH1 ELISA Kits) signaling
the synaptic localization of APP (show APP ELISA Kits), ADAM10 (show ADAM10 ELISA Kits), and BACE1 in the mouse cerebral cortex, was examined.
study demonstrates that SEZ6 and SEZ6L are physiological BACE1 substrates in the murine brain and suggests that sSEZ6 and sSEZ6L levels in CSF (show CSF2 ELISA Kits) are suitable markers to monitor BACE1 inhibition in mice
Chronic variable stress led to increased Bace1 expression in the hippocampus of young adult mice and the hippocampus, prefrontal cortex and amygdala of aged mice. The increased expression of Bace1 was associated with decreased methylation of several CpGs in the Bace1 promoter region.
In conclusion, glucocorticoid couples mGR with Galphas (show GNAS ELISA Kits) and triggers cAMP-PKA-CREB (show CREB1 ELISA Kits) axis dependent on the lipid raft to stimulate BACE1 upregulation and Abeta (show APP ELISA Kits) generation.SIGNIFICANCE STATEMENT Patients with Alzheimer's disease (AD) have been growing sharply and stress is considered as the major environment factor of AD.
study supports the hypothesis that Abeta (show APP ELISA Kits) induces microtubule disruption in presynaptic dystrophic neurites that surround plaques, thus impairing axonal transport and leading to accumulation of BACE1 and exacerbation of amyloid pathology in Alzheimer's disease
Here, we demonstrate that Snapin (show SNAPIN ELISA Kits)-mediated retrograde transport plays a critical role in removing BACE1 from presynaptic terminals toward the soma, thus reducing synaptic Abeta (show APP ELISA Kits) production. Adeno (show ADORA2A ELISA Kits)-associated virus-mediated Snapin (show SNAPIN ELISA Kits) overexpression in the hippocampus of mutant hAPP mice significantly decreases synaptic Abeta (show APP ELISA Kits) levels, attenuates synapse loss, and thus rescues cognitive deficits. Our study uncovers a new pathway...
beta-site APP cleaving enzyme 1 (BACE1) is essential for amyloid beta protein production. We discovered that A673V mutation shifted the BACE1 cleavage site from the Glu (show GCG ELISA Kits)(11) to the Asp(1 (show BACE2 ELISA Kits)) site, resulting in much higher C99 level and C99/C89 ratio.
bace1 mutants display hypomyelination in the peripheral nervous system and supernumerary neuromasts while in bace2 (show BACE2 ELISA Kits) mutants the shape and migration of melanocytes is affected.
Cerebral deposition of amyloid beta peptide is an early and critical feature of Alzheimer's disease. Amyloid beta peptide is generated by proteolytic cleavage of amyloid precursor protein (APP) by two proteases, one of which is the protein encoded by this gene. The encoded protein, a member of the peptidase A1 protein family, is a type I integral membrane glycoprotein and aspartic protease that is found mainly in the Golgi. Multiple transcript variants encoding different isoforms have been described for this gene.
, asp 2
, aspartyl protease 2
, beta-secretase 1
, beta-secretase 1 precursor variant 1
, beta-site APP cleaving enzyme 1
, beta-site amyloid beta A4 precursor protein-cleaving enzyme
, membrane-associated aspartic protease 2
, transmembrane aspartic proteinase Asp2
, beta-site amyloid precursor protein cleaving enzyme 1
, beta-site APP cleaving enzyme
, beta secretase 1
, beta-secretase 1 isoform A preproprotein
, beta-secretase 1 isoform B preproprotein
, beta-secretase 1 isoform C preproprotein
, beta-site APP-cleaving enzyme 1
, beta-secretase 1-like
, beta-site APP-cleaving enzyme 2
, beta-secretase 2-like