Search results for alpha

RELM alpha antibody, Genetex, GTX00822

HP1 alpha antibody, Genetex, GTX00897

CD8 alpha antibody, Genetex, GTX03377

Nucleolin, alpha antibody, Covalab, Ref 00029759

MRCK alpha antibody, Genetex, GTX102598

PP2A alpha antibody, Genetex, GTX106334

alpha Tubulin antibody, Genetex, GTX108784

PPARA/PPAR alpha, Bioss, bsm-55599r-100ul

alpha-tubulin Antibody, Abbexa, abx140218

alpha-tubulin Antibody is a Mouse Monoclonal against alpha-tubulin.

GSK3 alpha Antibody, Abbexa, abx033883

Glycogen synthase kinase 3-alpha (GSK3A) is a multifunctional protein serine kinase implicated in the control of several regulatory proteins including glycogen synthase and transcription factors. It also plays a role in the WNT and PI3K signaling pathways.1 Under resting conditions GSK3A and its homologs are highly phosphorylated at tyr279 in the phosphorylation loop.2 Constitutive phosphorylation of this tyrosine is important for kinase activity. Dephosphorylation of tyr279 after mitogen activation is accompanied by kinase inactivation. PKA as well as PI3K-activated PKB inactivate GSK3A by phosphorylation at ser21.3 Lysophosphatidic acid primarily utilizes a PKC-dependent pathway to modulate GSK3 and certain growth factors (e.g., PDGFB), which control GSK3 mainly through PIK3-PKB, are able to regulate GSK3 through an alternative, redundant phospholipase-C-gamma-PKC pathway.4 Alzheimer disease (AD) is associated with increased production and aggregation of amyloid-beta-40 and 42 peptides into plaques. GSK3A is required for maximal production of the beta-amyloid-40 and 42 peptides generated from the amyloid precursor protein (APP) by presenilin (PSEN1) dependent gamma-secretase cleavage.5 In vitro, lithium, a GSK3A inhibitor, blocked the production of the beta-amyloid peptides by interfering with the gamma-secretase step. In mice expressing familial AD-associated mutations in APP and PSEN1, lithium reduced the levels of beta-amyloid peptides GSK3A also phosphorylates the tau protein (MAPT), the principal component of neurofibrillary tangles in AD, and suggested that inhibition of GSK3A may offer a new therapeutic approach to AD.