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Published on: April 11, 2011
Early embryonic lethality caused by targeted disruption of the TRAF-interacting protein (TRIP) gene
Eui-Soon Park1, Seunga Choi, Jin-Man Kim
1Department of Microbiology and BK21 BioBC, Chungnam National University, Daejeon 305-764, Republic of Korea.
Abstract:
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.
Insights
TRAF-interacting protein (TRIP) is crucial for early embryonic development. TRIP deficiency in mice leads to embryonic lethality due to impaired cell proliferation and increased cell death, highlighting its essential in vivo role.
Area of Science:
- Molecular Biology
- Developmental Biology
- Immunology
Background:
- Tumor necrosis factor receptor (TNFR)-associated factors (TRAFs) are adaptor proteins mediating TNFR signaling.
- TRAF-interacting protein (TRIP) regulates TNF-induced NF-kappaB signaling and interacts with CYLD in vitro.
- The in vivo function of TRIP in development remained largely unknown.
Purpose of the Study:
- To elucidate the in vivo role of TRIP in early embryonic development.
- To investigate the consequences of TRIP deficiency in a whole organism model.
Main Methods:
- Generation of TRIP-deficient mice.
- Analysis of embryonic development in homozygous TRIP-deficient embryos.
Main Results:
- Homozygous TRIP-deficient mouse embryos exhibited embryonic lethality shortly after implantation.
- Deficiency in TRIP resulted in significant proliferation defects.
- Excessive cell death was observed in TRIP-deficient embryos.
Conclusions:
- TRIP is essential for normal early mouse embryonic development in vivo.
- TRIP plays a critical role in regulating cell proliferation and preventing excessive cell death during embryogenesis.
