Sign up for Table of Contents Alerts.
Email this page
Print this page
Extra Views
Genetic Deficiency of p38α Reveals its Critical Role in Myoblast Cell Cycle Exit:The p38α-JNK Connection
Eusebio Perdiguero, Vanessa Ruiz-Bonilla, Antonio L. Serrano and Pura Muñoz-Cánoves
volume 6 | issue 11
1 June 2007Pages: 1298 - 1303
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.
The regulation of skeletal muscle formation (myogenesis) is essential for normal development as well as in pathological conditions such as muscular dystrophies and inflammatory myopathies. Findings published over the past years have established a key role for the p38 MAP kinase signaling pathway in the control of muscle gene expression and myotube formation. However, the relative contribution of the four p38 MAP kinases (p38α, p38β, p38γ and p38δ) to this process was unknown. We have recently demonstrated that myoblasts lacking p38α, but not those lacking p38β or p38δ, were unable to differentiate and form multinucleated myotubes, while p38γ-deficient myoblasts exhibited an attenuated fusion capacity. Defective myogenesis in the absence of p38α was attributed to delayed cell cycle exit and continuous proliferation in differentiation-promoting conditions, caused by enhanced activation of the JNK/cJun pathway. We discuss these findings in the context of the emerging crosstalk of p38 and JNK signaling pathways in controlling cell growth and differentiation.
Authors
Eusebio Perdiguero
Center for Genomic Regulation, Barcelona, Spain
Vanessa Ruiz-Bonilla
Center for Genomic Regulation, Barcelona, Spain
Antonio L. Serrano
Center for Genomic Regulation, Barcelona, Spain
Pura Muñoz-Cánoves
Center for Genomic Regulation, Barcelona, Spain
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.