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First published online June 14, 2004

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Prohibitin' muscle differentiation

Muscle differentiation, like many aspects of development, is controlled by interplay between different signalling molecules and cell fate determinants. The MyoD and MEF2 transcription factors play key roles in the process, as does signalling by insulin-like growth factors (IGFs), which activate the kinases PI3K and Akt (also known as PKB). On p. 3021, Zhenguo Wu and coworkers establish a link between these myogenic regulators and along the way uncover a role for prohibitin 2 (PHB2) - a highly conserved protein whose function has so far remained elusive. Picking up PHB2 in two-hybrid screens for Akt-binding partners, the authors demonstrate that it is a transcriptional repressor that can inhibit MyoD- and MEF2-dependent transcription in C2C12 myoblasts and block muscle differentiation. They also show that it interacts with endogenous MyoD and MEF2 and inhibits transcription by recruiting the histone deacetylase HDAC1. Wu and coworkers go on to reveal that Akt promotes muscle differentiation by disrupting binding of PHB2 to MyoD, which allows the transcription factor to execute its function. Their findings therefore highlight a lesser-known aspect of Akt function: its kinase-independent effects.

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Akt binds prohibitin 2 and relieves its repression of MyoD and muscle differentiation

Luguo Sun, Lanying Liu, Xiang-Jiao Yang, and Zhenguo Wu
JCS 2004 117: 3021-3029. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?