期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 102, 期 38, 页码 13484-13489出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0504420102
关键词
GTPase-activating protein; Rho GTPases
资金
- NCI NIH HHS [R01 CA105117, CA 105117] Funding Source: Medline
- NIGMS NIH HHS [GM 60523, R01 GM060523] Funding Source: Medline
Rho family GTPase Cdc42 is known to regulate polarity and growth in lower eukaryotes, but its physiologic function in mammals has yet to be determined. Here we have disrupted cdc42gap, a ubiquitously expressed negative regulator of Cdc42, in, mice. Cdc42GAP(-/-) embryonic fibroblasts and various organs displayed significantly elevated Cdc42 activity. The embryonic and neonatal homozygous mice were reduced in size by approximate to 25-40% and suffered severe growth retardation. Major organs from Cdc42GAP(-/-) mice were proportionally smaller because of decreased cell number. Basal apoptosis was increased in Cdc42GAP(-/-) cells and tissues, and this was attributed to altered c-Jun N-terminal kinase apoptotic signals. These results reveal a role of Cdc42GAP in mammalian perinatal growth and implicate the c-Jun N-terminal kinase-mediated apoptosis machinery as a Cdc42 effector pathway in vivo.
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