期刊
JOURNAL OF CELL BIOLOGY
卷 168, 期 1, 页码 29-33出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200409067
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- NCI NIH HHS [CA93855, K01 CA093855, CA107548, R01 CA089209, CA89209, R01 CA107548] Funding Source: Medline
W e 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 NFKB 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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