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Product Name GSK3A Chinese Name 糖原合酶激酶3α抗体 Alias GSK3A_HUMAN; Glycogen synthase kinase-3 alpha; Glycogen synthase kinase 3 alpha; EC:2.7.11.26; Serine/threonine-protein kinase GSK3A; EC:2.7.11.1; GSK 3 alpha; GSK3alpha; GSK-3 alpha; GSK3 alpha; GSK-3alpha; GSK 3A; Immunogen Species Rabbit Clonality Polyclonal React Species (predicted: Human, Rat, ) Applications WB=1:500-1:1000
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.Theoretical molecular weight 54kDa Cellular localization The nucleus The cell membrane Form Liquid Concentration 1mg/ml Lsotype IgG2a/Kappa Purification Affinity purified by Protein A Buffer Solution 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Storage Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. Attention This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. PubMed PubMed Product Detail This gene encodes a multifunctional Ser/Thr protein kinase that is implicated in the control of several regulatory proteins including glycogen synthase, and transcription factors, such as JUN. It also plays a role in the WNT and PI3K signaling pathways, as well as regulates the production of beta-amyloid peptides associated with Alzheimer's disease. [provided by RefSeq, Oct 2011]
SWISS:
P49840
Gene ID:
2931
Database links:Entrez Gene: 2931 Human
SwissProt: P49840 Human
组成性活性蛋白激酶,通过磷酸化和失活糖原合成酶(GYS1或GYS2)、CTNNB1/β连环蛋白、APC和AXIN1,在激素控制葡萄糖稳态、Wnt信号传导和转录因子及微管的调节中作为负调节因子。它的大多数底物需要启动磷酸化。通过磷酸化和抑制GYS1活性从而促进糖原合成的胰岛素调节。调节肝脏的糖原代谢,而不是肌肉。也可能通过调节转录因子的激活来介导胰岛素抵抗的发展。在Wnt信号中,调节核CTNNB1/β连环蛋白的水平和转录活性。促进淀粉样前体蛋白(APP)的加工和阿尔茨海默病APP源性淀粉样斑块的形成。可能参与胰腺β细胞复制的调控。也是建立神经元极性和轴突生长所必需的。Product Picture Blocking buffer: 5% NFDM/TBST
Primary ab dilution: 1:1000
Primary ab incubation condition: 2 hours at room temperature
Secondary ab: Goat Anti-Rat IgG H&L (HRP)
Lysate: 293, U87MG
Protein loading quantity: 20 μg
Exposure time: 60 s
Predicted MW: 51 kDa
Observed MW: 51 kDa
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