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pubmed-article:17292329pubmed:abstractTextConstitutive activity of NF-kappaB is associated with various human cancers including adult T-cell leukemia (ATL). In this study, we have found Tgat that activates NF-kappaB by screening a cDNA expression library derived from ATL cells. We previously identified Tgat as the oncogene, which consists of the Rho-guanine nucleotide exchange factor (Rho-GEF) domain and the unique C-terminal region, as a consequence of alternative splicing of the Trio transcript. Tgat activated the IKK activity by binding with the IkappaB kinase (IKK) complex. The Tgat mutants lacking the C-terminal region failed to associate with the IKK complex suggesting an essential role of the unique sequence. The mutation causing the loss of GEF activity also abolished the NF-kappaB activation. Moreover, co-expressed p100 was efficiently processed into p52 in the Tgat-expressing cells, suggesting the co-involvement of non-canonical pathway.lld:pubmed
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pubmed-article:17292329pubmed:authorpubmed-author:KatamineShige...lld:pubmed
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pubmed-article:17292329pubmed:pagination269-74lld:pubmed
pubmed-article:17292329pubmed:dateRevised2009-11-19lld:pubmed
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pubmed-article:17292329pubmed:year2007lld:pubmed
pubmed-article:17292329pubmed:articleTitleTgat, a Rho-specific guanine nucleotide exchange factor, activates NF-kappaB via physical association with IkappaB kinase complexes.lld:pubmed
pubmed-article:17292329pubmed:affiliationDepartment of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan.lld:pubmed
pubmed-article:17292329pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:17292329pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed