Does GSK-3 provide a shortcut for PI3K activation of Wnt signalling?
Does GSK-3 provide a shortcut for PI3K activation of Wnt signalling?
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DOI：
10.3410/b2-82
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发表时间：
2010-11-24
期刊：
影响因子：
--
通讯作者：
Woodgett JR
中科院分区：
文献类型：
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作者：
Voskas D;Ling LS;Woodgett JR
糖原合成酶激酶-3（GSK-3）是磷脂酰肌醇3-激酶（PI 3 K）信号通路的公认下游组分，但也是负调节经典Wnt/β-连环蛋白信号通路的关键酶。最近的几项研究认为，PKB（蛋白激酶B）介导的GSK-3抑制导致β-连环蛋白的积累，但这两条途径之间是否真的存在串扰仍有争议。为了阐明共享信号传导组分的机制，需要进一步研究PI 3 K信号传导途径的不同组分和GSK-3或β-连环蛋白的不同池。
Glycogen synthase kinase-3 (GSK-3) is a well-established downstream component of the phosphatidylinositol 3-kinase (PI3K) signalling pathway but is also a key enzyme in negatively regulating the canonical Wnt/β-catenin signalling pathway. Several recent studies argue that PKB (protein kinase B)-mediated inhibition of GSK-3 leads to β-catenin accumulation, but whether cross-talk actually exists between these two pathways is controversial. To elucidate the mechanisms of shared signalling components, further studies taking into account different components of the PI3K signalling pathway and different pools of GSK-3 or β-catenin are required.