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Early embryonic lethality caused by targeted disruption of the TRAF-interacting protein (TRIP) gene.

Park ES, Choi S, Kim JM, Jeong Y, Choe J, Park CS, Choi Y, Rho J

Department of Microbiology and BK21 BioBC, Chungnam National University, Daejeon 305-764, Republic of Korea.

Tumor necrosis factor receptor (TNFR)-associated factors (TRAFs) are key adaptor molecules in the TNFR-signaling complexes that promote a wide variety of signaling cascades including cell proliferation, activation, differentiation, and apoptosis. TRAF-interacting protein (TRIP) is required for the inhibitory regulation of TNF-induced NF-kappaB signaling via the TNFR/TRAF-signaling complexes in vitro. TRIP also directly interacts with the familial cylindromatosis tumor suppressor gene (CYLD) and negatively regulates NF-kappaB activation in vitro. However, although there appears to be a relationship between TRIP, the TRAFs and also CYLD as modulators of NF-kappaB signaling in vitro, the functional role of TRIP in vivo is still unclear. To identify the role of TRIP in vivo, we have generated TRIP-deficient mice. Homozygous mouse embryos were found to die shortly after implantation due to proliferation defects and excessive cell death. These results indicate that TRIP is an essential factor during early mouse embryonic development in vivo.

Published 17 October 2007 in Biochem Biophys Res Commun, 363(4): 971-7.
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