Journal
MOLECULAR BIOLOGY OF THE CELL
Volume 22, Issue 8, Pages 1389-1397Publisher
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E10-10-0827
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Funding
- Ministry of Science and Technology of Shanghai [09XD1404800]
- National Natural Science Foundation of China [31030021]
- Ministry of Science and Technology of China [2010CB529703, 2011CB910904, 2007CB914504]
- Chinese Academy of Sciences [KSCX1-YW-R-06]
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Proteins that directly regulate tumor necrosis factor (TNF) signaling have critical roles in determining cell death and survival. Previously we characterized ubiquitously expressed transcript (UXT)-V2 as a novel transcriptional cofactor to regulate nuclear factor-kappa B in the nucleus. Here we report that another splicing isoform of UXT, UXT-V1, localizes in cytoplasm and regulates TNF-induced apoptosis. UXT-V1 knockdown cells are hypersensitive to TNF-induced apoptosis. We demonstrated that UXT-V1 is a new component of TNF receptor signaling complex. We found that UXT-V1 binds to TNF receptor-associated factor 2 and prevents TNF receptor-associated death domain protein from recruiting Fas-associated protein with death domain. More importantly, UXT-V1 is a short-half-life protein, the degradation of which facilitates the formation of the apoptotic receptor complex II in response to TNF treatment. This study demonstrates that UXT-V1 is a novel regulator of TNF-induced apoptosis and sheds new light on the underlying molecular mechanism of this process.
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