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Cerebral deposition of amyloid beta peptide is an early and critical feature of Alzheimer's disease and a frequent complication of Down syndrome. Additionally we are shipping beta-Site APP-Cleaving Enzyme 1 Kits (56) and beta-Site APP-Cleaving Enzyme 1 Proteins (34) and many more products for this protein.
Showing 10 out of 267 products:
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 - ABIN4900526
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 - ABIN4900525
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 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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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 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
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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Results indicate that SNX4 (show SNX4 Antibodies)-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.
In conclusion, glucocorticoid couples mGR (show GRHL1 Antibodies) with Galphas (show GNAS Antibodies) and triggers cAMP-PKA-CREB (show CREB1 Antibodies) axis dependent on the lipid raft to stimulate BACE1 upregulation and Abeta (show APP Antibodies) 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 Antibodies) 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 Antibodies)-mediated retrograde transport plays a critical role in removing BACE1 from presynaptic terminals toward the soma, thus reducing synaptic Abeta (show APP Antibodies) production. Adeno (show ADORA2A Antibodies)-associated virus-mediated Snapin (show SNAPIN Antibodies) overexpression in the hippocampus of mutant hAPP mice significantly decreases synaptic Abeta (show APP Antibodies) 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 Antibodies)(11) to the Asp(1 (show BACE2 Antibodies)) site, resulting in much higher C99 level and C99/C89 ratio.
SEPT8 (show SEPT8 Antibodies) modulates beta-amyloidogenic processing of APP (show APP Antibodies) through a mechanism affecting the intracellular sorting and accumulation of BACE1.
the depletion of BIN1 (show BIN1 Antibodies) 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 Antibodies) in the pathogenesis of Alzheimer disease (AD), as a novel genetic regulator of BACE1 levels and Ab production
In an Alzheimer's disease mouse model we show that BACE-1 is upregulated at the blood-brain barrier compared to healthy controls.
study provides new insights into autophagy-mediated regulation of BACE1 turnover and APP (show APP Antibodies) processing, thus building a foundation for future development of potential Alzheimer's disease therapeutic strategies.
analysis suggests that some familial Alzheimer's disease mutations in APP (show APP Antibodies) are amyloidogenic and/or amyloidolytic via selection of alternative BACE1 cleavage sites
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 Antibodies)/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.
in vitro BACE1-activity assays demonstrate that palmitoylation-dependent dimerization of APP (show APP Antibodies) promotes beta-cleavage of APP (show APP Antibodies) in lipid-rich detergent resistant cell membranes (DRMs), when compared to total APP (show APP Antibodies).
The circular RNA ciRS-7 promotes APP (show APP Antibodies) and BACE1 degradation in an NF-kappaB (show NFKB1 Antibodies)-dependent manner.
rs638405 in BACE1 was not associated with the risk of Alzheimer's disease (AD), rs638405 decreased the risk of apolipoprotein-E (show APOE Antibodies) 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.
bace1 mutants display hypomyelination in the peripheral nervous system and supernumerary neuromasts while in bace2 (show BACE2 Antibodies) 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.
beta-site APP-cleaving enzyme 1
, beta-secretase 1
, beta-secretase 1 isoform A preproprotein
, beta-secretase 1 isoform B preproprotein
, beta-secretase 1 isoform C preproprotein
, beta-secretase 1-like
, beta-site APP-cleaving enzyme 2
, beta-secretase 2-like
, APP beta-secretase
, asp 2
, aspartyl protease 2
, beta-site amyloid precursor protein cleaving enzyme 1
, membrane-associated aspartic protease 2
, beta-secretase 1 precursor variant 1
, beta-site APP cleaving enzyme 1
, beta-site amyloid beta A4 precursor protein-cleaving enzyme
, transmembrane aspartic proteinase Asp2
, beta-site APP cleaving enzyme
, beta secretase 1