Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10814799 | Cellular Signalling | 2015 | 9 Pages |
Abstract
We found that, in neonatal rat ventricular cardiomyocytes, ENH1 interacts with CREB, is necessary for the phosphorylation of CREB at ser133, and the activation of CREB-dependent transcription. On the contrary, the overexpression of ENH3, a LIM-less splice variant, inhibited the phosphorylation of CREB. ENH3 overexpression or shRNA knockdown of ENH1 prevented the CREB-dependent transcription. Our results thus suggest that ENH1 plays an essential role in CREB's activation and dependent transcription in cardiomyocytes. At the opposite, ENH3 prevents the CREB transcriptional activity. In conclusion, these results provide a first molecular explanation to the opposing functions of ENH splice variants.
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Authors
Jumpei Ito, Masumi Iijima, Nobuo Yoshimoto, Tomoaki Niimi, Shun'ichi Kuroda, Andrés D. Maturana,