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Cerebral deposition of amyloid beta peptide is an early and critical feature of Alzheimer's disease. 再加上，我们可以发beta-Site APP-Cleaving Enzyme 1 试剂盒 (62) 和 beta-Site APP-Cleaving Enzyme 1 蛋白 (31)和数多这个蛋白质的别的产品。
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Human Polyclonal BACE Primary Antibody for IF (p), IHC (p) - ABIN725705
Tian, Guo, Wu, Ma, Zhao: Minocycline Alleviates Sevoflurane-Induced Cognitive Impairment in Aged Rats. in Cellular and molecular neurobiology 2015
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Human Monoclonal BACE Primary Antibody for CyTOF, FACS - ABIN4900525
Cheng, He, Lee, Yao, Li, Shen: High activities of BACE1 in brains with mild cognitive impairment. in The American journal of pathology 2013
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Human Monoclonal BACE Primary Antibody for CyTOF, FACS - ABIN4900526
Ahmed, Holler, Webb, Li, Beckett, Murphy: BACE1 and BACE2 enzymatic activities in Alzheimer's disease. in Journal of neurochemistry 2010
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Human Polyclonal BACE Primary Antibody for WB - ABIN550289
Vassar, Bennett, Babu-Khan, Kahn, Mendiaz, Denis, Teplow, Ross, Amarante, Loeloff, Luo, Fisher, Fuller, Edenson, Lile, Jarosinski, Biere, Curran, Burgess, Louis, Collins, Treanor, Rogers, Citron: Beta-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE. in Science (New York, N.Y.) 1999
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Human Monoclonal BACE Primary Antibody for IHC, WB - ABIN4282833
Prior, Dargusch, Ehren, Chiruta, Schubert: The neurotrophic compound J147 reverses cognitive impairment in aged Alzheimer's disease mice. in Alzheimer's research & therapy 2014
Cow (Bovine) Polyclonal BACE Primary Antibody for IHC (p) - ABIN2477571
Rossner, Lange-Dohna, Zeitschel, Perez-Polo: Alzheimer's disease beta-secretase BACE1 is not a neuron-specific enzyme. in Journal of neurochemistry 2005
Human Polyclonal BACE Primary Antibody for IHC (p), WB - ABIN392201
Xie, Guo: PAR-4 is involved in regulation of beta-secretase cleavage of the Alzheimer amyloid precursor protein. in The Journal of biological chemistry 2005
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Endosome-to-TGN (显示 TG 抗体) trafficking of BACE1 is regulated by Par3 (显示 F2RL2 抗体) and aPKC. This is a mechanism in pathogenesis of Alzheimer disease.
Results indicate that SNX4 (显示 SNX4 抗体)-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 (显示 ADAM10 抗体)/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 (显示 SEPT8 抗体) modulates beta-amyloidogenic processing of APP (显示 APP 抗体) through a mechanism affecting the intracellular sorting and accumulation of BACE1.
the depletion of BIN1 (显示 BIN1 抗体) 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 (显示 BIN1 抗体) 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 (显示 APP 抗体) promotes beta-cleavage of APP (显示 APP 抗体) in lipid-rich detergent resistant cell membranes (DRMs), when compared to total APP (显示 APP 抗体).
The circular RNA ciRS-7 promotes APP (显示 APP 抗体) and BACE1 degradation in an NF-kappaB (显示 NFKB1 抗体)-dependent manner.
rs638405 in BACE1 was not associated with the risk of Alzheimer's disease (AD), rs638405 decreased the risk of apolipoprotein-E (显示 APOE 抗体) epsilon4 (APOE4) positive AD patients, rs638405 also decreased the risk of Asian AD patients. Data of meta-analysis suggested rs638405 in BACE1 was a protective factor of AD.
the synaptic localization of APP (显示 APP 抗体), ADAM10 (显示 ADAM10 抗体), and BACE1 in the mouse cerebral cortex, was examined.
study demonstrates that SEZ6 and SEZ6L (显示 SEZ6L 抗体) are physiological BACE1 substrates in the murine brain and suggests that sSEZ6 and sSEZ6L levels in CSF (显示 CSF2 抗体) 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 (显示 GRHL1 抗体) with Galphas (显示 GNAS 抗体) and triggers cAMP-PKA-CREB (显示 CREB1 抗体) axis dependent on the lipid raft to stimulate BACE1 upregulation and Abeta (显示 APP 抗体) 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 (显示 APP 抗体) 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 (显示 SNAPIN 抗体)-mediated retrograde transport plays a critical role in removing BACE1 from presynaptic terminals toward the soma, thus reducing synaptic Abeta (显示 APP 抗体) production. Adeno (显示 ADORA2A 抗体)-associated virus-mediated Snapin (显示 SNAPIN 抗体) overexpression in the hippocampus of mutant hAPP mice significantly decreases synaptic Abeta (显示 APP 抗体) 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 (显示 GCG 抗体)(11) to the Asp(1 (显示 BACE2 抗体)) 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 (显示 BACE2 抗体) 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