Cdk9-55: A new player in muscle regeneration

Adult skeletal muscle contains a specialized population of myogenic quiescent stem cells, termed satellite cells, which contribute to repair myofibers after injury. During muscle regeneration, satellite cells exit their normal quiescent state, proliferate, activating MyoD and Myf‐5 expression, and f...

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Published inJournal of cellular physiology Vol. 216; no. 3; pp. 576 - 582
Main Authors Giacinti, Cristina, Musarò, Antonio, De Falco, Giulia, Jourdan, Isabelle, Molinaro, Mario, Bagella, Luigi, Simone, Cristiano, Giordano, Antonio
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.09.2008
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Summary:Adult skeletal muscle contains a specialized population of myogenic quiescent stem cells, termed satellite cells, which contribute to repair myofibers after injury. During muscle regeneration, satellite cells exit their normal quiescent state, proliferate, activating MyoD and Myf‐5 expression, and finally differentiate and fuse to reconstitute the injured muscle architecture. We have previously reported that cdk9 is required for myogenesis in vitro by activating MyoD‐dependent transcription. In myoblasts induced to differentiate, MyoD recruits cdk9 on the chromatin of muscle‐specific regulatory regions. This event correlates with chromatin‐modifying enzyme recruitment and phosphorylation of cdk9‐specific target residues at the carboxyl‐terminal domain of RNA polymerase II. Here we report that a second cdk9 isoform, termed cdk9‐55, plays a fundamental role in muscle regeneration and differentiation in vivo. This alternative form is specifically induced in injured myofibers and its activity is strictly required for the completion of muscle regeneration process. J. Cell. Physiol. 216: 576–582, 2008, © 2008 Wiley‐Liss, Inc.
Bibliography:Sbarro Health Research Organization
ark:/67375/WNG-5637F3GC-T
NIH
istex:8C12B4FBD03E2301D349ADF630EB589FB11A1429
ArticleID:JCP21361
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.21361