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    1. PI3K/Akt/mTOR
      Stem Cell/Wnt
    2. GSK-3


    Glycogen synthase kinase 3 (GSK-3) is a multifunctional serine/threonine kinase found in all eukaryotes. GSK-3 is one of the few signaling mediators that play central roles in a diverse range of signaling pathways, including those activated by Wnts, hedgehog, growth factors, cytokines, and G protein-coupled ligands. GSK-3 targets transcription factors, regulates the activity of metabolic and signaling enzymes, and controls the half-life of proteins by earmarking them for degradation. GSK-3 exists as two isoforms, GSK-3a (51 kDa) and GSK3b (47 kDa), which are encoded by distinct genes. These isoforms often have overlapping functions, but they do not always compensate for each other.

    View GSK-3 Pathway Map

    GSK-3 Isoform Specific Products:

    • GSK-3

    • GSK-3α

    • GSK-3β

    GSK-3 相关产品 (24):

    Cat. No. Product Name Effect Purity
    • HY-10182
      CHIR-99021 Inhibitor 99.76%
      CHIR-99021是 GSK-3α/β 抑制剂, IC50 分别为 10 nM,6.7 nM。 抑制 GSK-3α/β 比同源物 CDC2 和 ERK2 高 500 倍。
    • HY-12012
      SB 216763 Inhibitor
      SB 216763是有效,选择性和ATP竞争性的 GSK-3 抑制剂,抑制GSK-3α和GSK-3β的 IC50 为34.3 nM。
    • HY-10590
      TWS119 Inhibitor >98.0%
      TWS119 是一种 GSK-3β 特异性抑制剂,IC50 值为 30 nM,同时可激活 wnt/β-catenin 信号通路。
    • HY-16294
      LY2090314 Inhibitor 99.75%
      LY2090314 是一种有效的 GSK-3 抑制剂,抑制 GSK-3α 和 GSK-3β,IC50 值分别为 1.5 nM 和 0.9 nM。
    • HY-14872
      Tideglusib Inhibitor 99.81%
      Tideglusib是一种不可逆的 GSK-3 抑制剂,抑制 GSK-3βWTGSK-3βC199AIC50 分别为5 nM,60 nM。
    • HY-15356
      BIO-acetoxime Inhibitor >98.0%
      BIO-acetoxime (BIA) 是一种有效、选择性的 GSK-3 抑制剂,对 GSK-3α/β 的 IC50 值均为 10 nM;BIO-acetoxime 具有抗惊厥和抗感染作用。
    • HY-12302
      Kenpaullone Inhibitor 98.07%
      Kenpaullone 是一种有效的 CDK1/cyclin BGSK-3β 抑制剂,IC50 值分别为 0.4 μM 和 23 nM,同时可抑制 CDK2/cyclin A,CDK2/cyclin E 和 CDK5/p25 的活性,IC50 值分别为 0.68 μM,7.5 μM 和 0.85 μM。
    • HY-10580
      GSK 3 Inhibitor IX Inhibitor 99.42%
      GSK 3 Inhibitor IX (6-Bromoindirubin-3'-oxime; BIO) 是一种有效的,选择性的,可逆的,ATP 竞争性的 GSK-3α/βCDK1-cyclinB 复合体抑制剂,能够抑制 (GSK-3α/β)/CDK1/CDK5 的活性,IC50 值分别为 5 nM/320 nM/83 nM。
    • HY-10512
      AR-A014418 Inhibitor
      AR-A014418 是一种有效,选择性,ATP 竞争性的 GSK3β 抑制剂,IC50 值为 104 nM。
    • HY-10182B
      CHIR-99021 trihydrochloride Inhibitor
      CHIR-99021 (CT99021) 是一个GSK-3α/β的抑制剂。
    • HY-15504A
      RGB-286638 free base Inhibitor 99.55%
      RGB-286638 是一种有效的 CDK 抑制剂,抑制 cyclin T1-CDK9cyclin B1-CDK1cyclin E-CDK2cyclin D1-CDK4cyclin E-CDK3p35-CDK5 活性,IC50 分别为 1,2,3,4,5 和 5 nM;同时可抑制 GSK-3β,TAK1,Jak2 和 MEK1,IC50
    • HY-13862
      AZD1080 Inhibitor 99.10%
      AZD1080 是一种有效的选择性 GSK3 抑制剂。AZD1080 抑制重组人 GSK3αGSK3βpKi (IC50) 分别为 8.2 (6.9 nM) 和 7.5 (31 nM)。
    • HY-15761
      AZD2858 Inhibitor 99.24%
      AZD2858 是一种有效的,可口服的 GSK-3 抑制剂,可以抑制 GSK-3αGSK-3β 的活性,IC50 值分别为 0.9 和 5 nM,可用于骨折愈合的研究。
    • HY-15438
      SB 415286 Inhibitor 99.88%
      SB 415286 是一种有效的 GSK-3α 抑制剂,IC50 值为 77.5 nM,Ki 值为 30.75 nM;SB 415286 对人 GSK-3αGSK-3β 的抑制效果相同。
    • HY-19807
      Indirubin-3'-monoxime Inhibitor 99.95%
      Indirubin-3'-monoxime 是一种有效的 GSK-3β 抑制剂,对 5-Lipoxygenase 的抑制作用较弱,IC50 值分别为 22 nM 和 7.8-10 μM;Indirubin-3'-monoxime 同时对 CDK5/p25 和 CDK1/cyclin B 也有较强作用,IC50 值分别为 100 和 180 nM。
    • HY-12524
      Bikinin Inhibitor 99.82%
      Bikinin 是一种非甾体类的,植物性 GSK-3/Shaggy-like kinases 的 ATP 竞争性抑制剂,可激活 BR 信号通路。
    • HY-13076
      CHIR-98014 Inhibitor >98.0%
      CHIR-98014 是一种有效的,细胞通透的 GSK-3 抑制剂,可抑制 GSK-3αGSK-3β 的活性,IC50 值分别为 0.65 和 0.58 nM;CHIR-98014 对 cdc2 和 erk2 的作用较弱。
    • HY-11012
      TDZD-8 Inhibitor 98.74%
      TDZD-8 是 GSK-3β 的抑制剂,IC50 为 2 μM;TDZD-8 对 Cdk-1/cyclin?B,CK-II,PKA 和 PKC 的作用较弱,IC50 值均 >100 μM。
    • HY-12292
      IM-12 Inhibitor
      IM-12 是 GSK-3β 的抑制剂,IC50 值为 53 nM,可增强 Wnt 信号传导。
    • HY-10182A
      CHIR-99021 monohydrochloride Inhibitor 99.93%
      CHIR-99021 (CT99021) 是一个GSK-3α/β的抑制剂。

    Glycogen synthase kinase 3 (GSK-3) is a multifunctional serine/threonine kinase found in all eukaryotes. GSK-3 is one of the few signaling mediators that play central roles in a diverse range of signaling pathways, including those activated by Wnt, PI3K, growth factors, cytokines, and ligands for G protein-coupled receptors. The PI3K pathway is known for regulating metabolism, cell growth, and cell survival. The PI3K activity is stimulated by diverse oncogenes and growth factor receptors. PI3K-mediated production of PIP3 leads to the activation of Akt. The activation of Akt leads to the phosphorylation of GSK-3, which is active in resting cells, but is inactivated by the phosphorylation. The GSK-3 has been linked to the regulation of an assembly of transcription factors, including β-catenin, NF-κB, c-Jun, CREB, and STAT. Thus, the altered activity of GSK-3 causes various effects on cytokine expression. 


    In the absence of Wnt signaling, β-catenin is phosphorylated by CK1 and GSK-3. This phosphorylation leads to recognition by β-TrCP, leading to the ubiquitylation of β-catenin and degradation by the proteasome. Upon binding of a lipid-modified Wnt protein to the receptor complex, a signaling cascade is initiated. LRP is phosphorylated by CK1/CK2 and GSK-3, and Axin is recruited to the plasma membrane. The kinases in the β-catenin destruction complex are inactivated and β-catenin translocates to the nucleus to form an active transcription factor complex with TCF, leading to transcription of a large set of target genes.


    Some endogenous growth factors could bind to and activate the tyrosine kinase receptor. This facilitates the recruitment of other proteins (SHC, SOS), which results in the activation of the ERK-MAPK cascade and the inhibition of GSK-3. GSK-3 exerts many cellular effects: it regulates cytoskeletal proteins, and is important in determining cell survival/cell death. GSK-3 has also been identified as a target for the actions of lithium. GSK-3 can inhibit glycogen synthase, the enzyme that catalyzes the transfer of glucose from UDPG to glycogen[1][2].



    [1]. Brenner D, et al. Regulation of tumour necrosis factor signalling: live or let die.Nat Rev Immunol. 2015 Jun;15(6):362-74. 
    [2]. Conrad M, et al. Regulated necrosis: disease relevance and therapeutic opportunities.Nat Rev Drug Discov. 2016 May;15(5):348-66. 

    Isoform Specific Products

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