Journal
JOURNAL OF BIOCHEMISTRY
Volume 151, Issue 6, Pages 563-571Publisher
OXFORD UNIV PRESS
DOI: 10.1093/jb/mvs040
Keywords
TGF-beta; EMT; ESRP alternative splicing
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Funding
- KAKENHI from the Ministry of Education, Culture, Sports, Science and Technology of Japan
- Grants-in-Aid for Scientific Research [22390052, 23390202] Funding Source: KAKEN
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Epithelial-mesenchymal transition (EMT) is a crucial event in appropriate embryonic development as well as in wound healing, tissue repair and cancer progression in adult tissues. EMT endows cells with migratory and invasive properties, inhibits apoptosis and senescence, contributes to immunosuppression and induces stress resistance and stem cell properties. Many secreted polypeptide factors act in a sequential or cooperative manner to elicit EMT. Transforming growth factor (TGF)-beta can initiate and maintain EMT by activating intracellular signalling pathways. Recent studies have provided new insights into molecular mechanisms by which TGF-beta mediates changes in transcription of EMT regulators and EMT marker proteins, as well as changes in alternative splicing controlled by epithelial splicing regulatory proteins 1 and 2. Here, we present some of the emerging molecular mechanisms that mediate EMT upon exposure to TGF-beta.
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