NDLI: Extracellular signal-regulated kinase 2 is necessary for mesoderm differentiation.

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Extracellular signal-regulated kinase 2 is necessary for mesoderm differentiation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Su, Michael S. S. Boucher, Diane M. Yao, Yao Li, Wei Wu, Junwei Germann, Ursula A. Kuida, Keisuke
Description	Author Affiliation: Yao Y ( Department of Biology, Vertex Pharmaceuticals, 130 Waverly Street, Cambridge, MA 02139, USA.);
Abstract	The extracellular signal-regulated kinase (ERK) is a component of the mitogen-activated protein kinase cascade. Exon 2 of erk2 was deleted by homologous recombination and resulted in embryonic lethality at embryonic day 6.5. erk2 mutant embryos did not form mesoderm and showed increased apoptosis but comparable levels of BrdUrd incorporation, indicating a defect in differentiation. erk2 null embryonic stem (ES) cells exhibited reduced total ERK activity upon serum stimulation, augmented ERK1 phosphorylation, and decreased downstream p90Rsk phosphorylation and activity; yet ES cell proliferation was unaffected. Mutant ES cells were capable of forming mesoderm; however, treatment of mutant ES cells with the mitogen-activated protein kinase kinase inhibitor PD184352 decreased total ERK activity and expression of the mesodermal marker brachyury, suggesting that ERK1 can compensate for ERK2 in vitro. Normal embryos at embryonic day 6.5 expressed activated ERK1/2 in the extraembryonic ectoderm, whereas erk2 mutant embryos had no detectable activated ERK1/2 in this region, suggesting that activated ERK1 was not expressed, and therefore cannot compensate for loss of ERK2 in vivo. These data indicate that ERK2 plays an essential role in mesoderm differentiation during embryonic development.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	22
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Differentiation Physiology Mesoderm Cytology Mitogen-Activated Protein Kinase 1 Metabolism Animals Benzamides Pharmacology Genetics Cell Division Cell Line Enzyme Inhibitors Heterozygote Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Antagonists & Inhibitors Deficiency Mitogen-Activated Protein Kinase 3 Mitogen-Activated Protein Kinases Stem Cells Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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