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Cerebral deposition of amyloid beta peptide is an early and critical feature of Alzheimer's disease. Zusätzlich bieten wir Ihnen beta-Site APP-Cleaving Enzyme 1 Antikörper (229) und beta-Site APP-Cleaving Enzyme 1 Kits (71) und viele weitere Produktgruppen zu diesem Protein an.
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Results indicated that the proinflammatory cytokine TNF-alpha impairs endothelial tight junctions and promotes monocyte-endothelial cell adhesion by upregulating beta-site amyloid precursor protein enzyme 1 expression through activating PKC signaling and sequentially cleaving alpha-2, 6-sialic acid transferase 1.
Study did not detect any difference in peripheral expression of BACE1 and its naturally occurring antisense in epileptic patients and healthy subjects but a significant correlation between the transcript levels of these genes.
BACE1 is predominantly SUMOylated at K501 residue, which escalates its protease activity and stability and subsequently increases Abeta (zeige APP Proteine) production.
Their anti-BACE1 and antimicrobial activity.
Structural arrangement of BACE1-TM trimers and a mechanism for copper ion conduction that might also apply to other proteins involved in metal ion transport.
Potentials for beneficial or consequential effects resulting from pharmacologic inhibition of BACE1 are reviewed in context of ongoing clinical trials testing the effect of BACE1 candidate inhibitor drugs in Alzheimer's disease populations.
Measured plasma levels of beta-secretase 1 (BACE1) long non-coding RNA(LncRNA) in Alzheimer disease (AD) patients and healthy controls; found plasma BACE1 LncRNA to be a specific biomarker for AD.
Amyloid beta oligomers modulate BACE1 through an XBP-1 (zeige XBP1 Proteine)-dependent pathway involving HRD1 (zeige SYVN1 Proteine).
Polymethoxyflavones isolated from citrus peels might be considered as promising BACE1 inhibitory agents that could lower Abeta (zeige APP Proteine) production in Alzheimer disease.
In BACE1 transgenic (Tg) mice, axonal regeneration was reduced when compared with wilde-type (WT) littermates at 3 and 10 days post crush. Study observed a decreased percentage of innervated neuromuscular junctions at 15 days post crush; and a functional recovery delay in the transgenic mice as it took 8 weeks for the compound muscle action potential amplitudes of Tg mice to begin to reach similar values comparable to WT.
BACE1 deficiency develops abnormal clusters of immature neurons, forming doublecortin (zeige DCX Proteine)-positive neuroblasts, in the developing dentate gyrus, mainly in the subpial zone.
Increased TNFR1 (zeige TNFRSF1A Proteine) expression and signaling in injured peripheral nerves of mice with reduced BACE1 activity
We aimed to explore the potential therapeutic effect of PGC-1alpha by generating a lentiviral vector to express human PGC-1alpha 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 (zeige APP Proteine) deposition, associated with a decrease in BACE1 expression
that BACE1 deficiency enhances proliferation of Schwann cell due to the elevated Jag1 (zeige JAG1 Proteine)/Delta1-Notch (zeige NOTCH1 Proteine) signaling
the synaptic localization of APP (zeige APP Proteine), ADAM10 (zeige ADAM10 Proteine), and BACE1 in the mouse cerebral cortex, was examined.
study demonstrates that SEZ6 and SEZ6L (zeige SEZ6L Proteine) are physiological BACE1 substrates in the murine brain and suggests that sSEZ6 and sSEZ6L levels in CSF (zeige CSF2 Proteine) 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.
Results indicate that SNX4 (zeige SNX4 Proteine)-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 (zeige GRHL1 Proteine) with Galphas (zeige GNAS Proteine) and triggers cAMP-PKA-CREB (zeige CREB1 Proteine) axis dependent on the lipid raft to stimulate BACE1 upregulation and Abeta (zeige APP Proteine) generation.SIGNIFICANCE STATEMENT Patients with Alzheimer's disease (AD) have been growing sharply and stress is considered as the major environment factor of AD.
bace1 mutants display hypomyelination in the peripheral nervous system and supernumerary neuromasts while in bace2 (zeige BACE2 Proteine) 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