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This Article Free via Open Access: OA OA Full Text Full Text (PDF) OA All Versions of this Article: 2006-0612v1 25/5/1090    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints/Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Binétruy, B. Articles by Aouadi, M. Search for Related Content PubMed PubMed Citation Articles by Binétruy, B. Articles by Aouadi, M.

EMBRYONIC STEM CELLS: CHARACTERIZATION SERIES

Concise Review: Regulation of Embryonic Stem Cell Lineage Commitment by Mitogen-Activated Protein Kinases

^aINSERM, U626, Marseille, France;
^bUniversité de Marseille II, Faculté de Médecine, Marseille, France;
^cDepartment of Medicine, University of Colorado Health Sciences Center, Denver, Colorado, USA;
^dINSERM, U568, Nice, France;
^eUniversité de Nice Sophia-Antipolis, Faculté de Médecine, Nice, France

Key Words. Mitogen-activated protein kinases • Embryonic stem cells commitment • c-Jun amino-terminal kinase pathway p38MAPK pathway • Extracellular signal-regulated kinase pathway

Correspondence: Bernard Binétruy, Ph.D., INSERM, U626, Faculté de Médecine, 27 Bd J Moulin, 13385 Marseille, France. Telephone: (33) 4 9132 4406; Fax: (33) 4 9125 4336; e-mail: Bernard.Binetruy{at}medecine.univ-mrs.fr

Received September 28, 2006; accepted for publication January 4, 2007.
First published online in STEM CELLS EXPRESS   January 11, 2007.



Embryonic stem (ES) cells can give rise, in vivo, to the ectodermal, endodermal, and mesodermal germ layers and, in vitro, can differentiate into multiple cell lineages, offering broad perspectives in regenerative medicine. Understanding the molecular mechanisms governing ES cell commitment is an essential challenge in this field. The mitogen-activated protein kinase (MAPK) pathways extracellular signal-regulated kinase (ERK), c-Jun amino-terminal kinase (JNK), and p38MAPK are able to regulate ES commitment from early steps of the process to mature differentiated cells. Whereas the ERK pathway inhibits the self-renewal of ES cells, upon commitment this pathway is involved in the development of extraembryonic tissues, in early mesoderm differentiation, and in the formation of mature adipocytes; p38MAPK displays a large spectrum of action from neurons to adipocytes, and JNK is involved in both ectoderm and primitive endoderm differentiations. Furthermore, for a given pathway, several of these effects are isoform-dependent, revealing the complexity of the cellular response to activation of MAPK pathways. Regarding tissue regeneration, the potential outcome of systematic analysis of the function of different MAPKs in different ES cell differentiation programs is discussed.

Disclosure of potential conflicts of interest is found at the end of this article.