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

Eui Soon Park; Seunga Choi; Jin Man Kim; Yongsu Jeong; Joonho Choe; Chang Sik Park; Yongwon Choi; Jaerang Rho

doi:10.1016/j.bbrc.2007.09.103

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

Eui Soon Park, Seunga Choi, Jin Man Kim, Yongsu Jeong, Joonho Choe, Chang Sik Park, Yongwon Choi, Jaerang Rho

Research output: Contribution to journal › Article › peer-review

38 Citations (Scopus)

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-κB 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-κB activation in vitro. However, although there appears to be a relationship between TRIP, the TRAFs and also CYLD as modulators of NF-κB 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.

Original language	English
Pages (from-to)	971-977
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	363
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2007.09.103
Publication status	Published - 30 Nov 2007

Bibliographical note

Funding Information:
We thank D. Kim, O. Lee, S. Park, M. Kang, J. Park, S. Jang, and J. Kim for their helpful discussions and technical assistance. This work was supported by a Korea Research Foundation Grant of the Korean Government (C00154, C00283 and BK21 Project), and by an RCTCP (R11-2002-100-02005-0) and R01-2006-000-10067-0 funded by KOSEF.

Keywords

Knockout mouse
Signal transduction
TNF
TRAF
TRIP

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10.1016/j.bbrc.2007.09.103

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title = "Early embryonic lethality caused by targeted disruption of the TRAF-interacting protein (TRIP) gene",

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-κB 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-κB activation in vitro. However, although there appears to be a relationship between TRIP, the TRAFs and also CYLD as modulators of NF-κB 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.",

keywords = "Knockout mouse, Signal transduction, TNF, TRAF, TRIP",

author = "Park, {Eui Soon} and Seunga Choi and Kim, {Jin Man} and Yongsu Jeong and Joonho Choe and Park, {Chang Sik} and Yongwon Choi and Jaerang Rho",

note = "Funding Information: We thank D. Kim, O. Lee, S. Park, M. Kang, J. Park, S. Jang, and J. Kim for their helpful discussions and technical assistance. This work was supported by a Korea Research Foundation Grant of the Korean Government (C00154, C00283 and BK21 Project), and by an RCTCP (R11-2002-100-02005-0) and R01-2006-000-10067-0 funded by KOSEF. ",

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AU - Park, Eui Soon

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AU - Kim, Jin Man

AU - Jeong, Yongsu

AU - Choe, Joonho

AU - Park, Chang Sik

AU - Choi, Yongwon

AU - Rho, Jaerang

N1 - Funding Information: We thank D. Kim, O. Lee, S. Park, M. Kang, J. Park, S. Jang, and J. Kim for their helpful discussions and technical assistance. This work was supported by a Korea Research Foundation Grant of the Korean Government (C00154, C00283 and BK21 Project), and by an RCTCP (R11-2002-100-02005-0) and R01-2006-000-10067-0 funded by KOSEF.

PY - 2007/11/30

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N2 - 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-κB 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-κB activation in vitro. However, although there appears to be a relationship between TRIP, the TRAFs and also CYLD as modulators of NF-κB 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.

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

Abstract

Bibliographical note

Keywords

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