| First Author | Wang L | Year | 2005 |
| Journal | Proc Natl Acad Sci U S A | Volume | 102 |
| Issue | 38 | Pages | 13484-9 |
| PubMed ID | 16157885 | Mgi Jnum | J:101418 |
| Mgi Id | MGI:3603987 | Doi | 10.1073/pnas.0504420102 |
| Citation | Wang L, et al. (2005) Cdc42GAP regulates c-Jun N-terminal kinase (JNK)-mediated apoptosis and cell number during mammalian perinatal growth. Proc Natl Acad Sci U S A 102(38):13484-9 |
| abstractText | 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 approximately 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. |
