Glycogen synthase kinase-3 is an endogenous inhibitor of Snail transcription: implications for the epithelial-mesenchymal transition.
Glycogen synthase kinase-3 is an endogenous inhibitor of Snail transcription: implications for the epithelial-mesenchymal transition.
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DOI：
10.1083/jcb.200409067
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发表时间：
2005-01-03
期刊：
影响因子：
--
通讯作者：
Mercurio AM
中科院分区：
文献类型：
--
作者：
Bachelder RE;Yoon SO;Franci C;de Herreros AG;Mercurio AM
我们报告，糖原合成酶激酶-3（GSK-3）的活性是维持上皮结构所必需的。在正常乳腺和皮肤上皮细胞中使用小干扰RNA对其活性进行药理学抑制或降低其表达，导致E-钙粘蛋白表达降低和更多的间充质形态，这两者都是与上皮-间充质转化（EMT）相关的特征。重要的是，GSK-3抑制还刺激Snail的转录，Snail是E-钙粘蛋白的阻遏物和EMT的诱导物。我们确定NFκB是一种在上皮细胞中受GSK-3抑制的转录因子，与Snail表达相关。这些发现表明，上皮细胞必须维持特定激酶的激活，以阻止间充质转化。
We report that the activity of glycogen synthase kinase-3 (GSK-3) is necessary for the maintenance of the epithelial architecture. Pharmacological inhibition of its activity or reducing its expression using small interfering RNAs in normal breast and skin epithelial cells results in a reduction of E-cadherin expression and a more mesenchymal morphology, both of which are features associated with an epithelial–mesenchymal transition (EMT). Importantly, GSK-3 inhibition also stimulates the transcription of Snail, a repressor of E-cadherin and an inducer of the EMT. We identify NFκB as a transcription factor inhibited by GSK-3 in epithelial cells that is relevant for Snail expression. These findings indicate that epithelial cells must sustain activation of a specific kinase to impede a mesenchymal transition.
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影响因子：
5.3
作者：
Carver, EA;Jiang, RL;Gridley, T
通讯作者：
Gridley, T
影响因子：
21.3
作者：
Batlle, E;Sancho, E;de Herreros, AG
通讯作者：
de Herreros, AG
DOI：
10.1186/bcr651
发表时间：
2003
期刊：
Breast cancer research : BCR
影响因子：
--
作者：
Kowalski PJ;Rubin MA;Kleer CG
通讯作者：
Kleer CG
影响因子：
7.8
作者：
Liebner, S;Cattelino, A;Dejana, E
通讯作者：
Dejana, E
影响因子：
--
作者：
Coghlan, MP;Culbert, AA;Holder, JC
通讯作者：
Holder, JC