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Content Provider | World Health Organization (WHO)-Global Index Medicus |
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Author | Sekine, Yuichi Kon, Shigeyuki Togi, Sumihito Matsuda, Tadashi Muromoto, Ryuta Souma, Yuki Shiga, Kaname Kato, Masaya Oritani, Kenji |
Description | Country affiliation: Japan Author Affiliation: Togi S ( Department of Immunology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0812, Japan.) |
Abstract | Although Y14 is known to be a component of the exon junction complex, we previously reported that Y14 regulates IL-6-induced STAT3 activation. In this study, we showed that endogenous Y14 positively regulated TNF- -induced IL-6 expression in HeLa cells. Small interfering RNA-mediated Y14-knockdown reduced TNF- -induced and NF-κB-mediated transcriptional activity, phosphorylation/degradation of IκB , and nuclear localization of NF-κB/p65. As in the case of IL-6 stimuli, Y14 enhanced TNF- -induced STAT3 phosphorylation, which is important for its nuclear retention. However, our manipulation of Y14 expression indicated that it is involved in TNF- -induced IL-6 expression via both STAT3-dependent and -independent mechanisms. We screened signaling molecules in the TNF- -NF-κB pathway and found that Y14 endogenously associated with receptor-interacting protein 1 (RIP1) and TNFR-associated death domain (TRADD). Overexpression of RIP1, but not TRADD, restored TNF- -induced NF-κB activation in Y14-knockdown cells, and Y14 overexpression restored TNF- -induced NF-κB activation in TRADD-knockdown cells, but not in RIP1-knockdown cells, indicating that Y14 lies downstream of TRADD and upstream of RIP1. Of importance, Y14 significantly enhanced the binding between RIP1 and TRADD, and this is a possible new mechanism for Y14-mediated modification of TNF- signals. Although Y14 associates with MAGOH in the exon junction complex, Y14's actions in the TNF- -NF-κB pathway are unlikely to require MAGOH. Therefore, Y14 positively regulates signals for TNF- -induced IL-6 production at multiple steps beyond an exon junction complex protein. |
ISSN | 00221767 |
e-ISSN | 15506606 |
Journal | The Journal of Immunology |
Issue Number | 3 |
Volume Number | 191 |
Language | English |
Publisher | The American Association of Immunologists |
Publisher Date | 2013-08-01 |
Publisher Place | United States |
Access Restriction | Open |
Subject Keyword | Nf-kappa B Metabolism Nuclear Pore Complex Proteins Rna-binding Proteins Tnf Receptor-associated Death Domain Protein Tumor Necrosis Factor-alpha Cell Line, Tumor Hek293 Cells Hela Cells I-kappa B Proteins Interleukin-6 Biosynthesis Genetics Nuclear Proteins Phosphorylation Promoter Regions, Genetic Rna Interference Rna, Small Interfering Stat1 Transcription Factor Stat3 Transcription Factor Tnf Receptor-associated Factor 2 Transcription Factor Rela Transcription, Genetic Research Support, Non-u.s. Gov't Discipline Immunology |
Content Type | Text |
Resource Type | Article |
Subject | Immunology and Allergy Immunology |
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