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糖原合成酶激酶3(GSK-3)是否为PI3K激活Wnt信号通路提供了一条捷径?

Does GSK-3 provide a shortcut for PI3K activation of Wnt signalling?

作者信息

Voskas Daniel, Ling Ling S, Woodgett James R

出版信息

F1000 Biol Rep. 2010 Nov 24;2:82. doi: 10.3410/B2-82.

DOI:10.3410/B2-82
PMID:21283602
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3026644/
Abstract

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.

摘要

糖原合酶激酶-3(GSK-3)是磷脂酰肌醇3激酶(PI3K)信号通路中一个已被充分证实的下游组分,但也是负向调节经典Wnt/β-连环蛋白信号通路的关键酶。最近的几项研究认为,蛋白激酶B(PKB)介导的对GSK-3的抑制会导致β-连环蛋白积累,但这两条通路之间是否实际存在相互作用仍存在争议。为阐明共享信号组分的机制,需要进一步开展研究,考虑PI3K信号通路的不同组分以及GSK-3或β-连环蛋白的不同库。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb8b/3026644/2804b84a7157/biolrep-02-82-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb8b/3026644/2804b84a7157/biolrep-02-82-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb8b/3026644/2804b84a7157/biolrep-02-82-g001.jpg

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