2003年12月
Role of the TAB2-related protein TAB3 in IL-1 and TNF signaling
EMBO JOURNAL
- ,
- ,
- ,
- ,
- ,
- 巻
- 22
- 号
- 23
- 開始ページ
- 6277
- 終了ページ
- 6288
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1093/emboj/cdg605
- 出版者・発行元
- OXFORD UNIV PRESS
The cytokines IL-1 and TNF induce expression of a series of genes that regulate inflammation through activation of NF-kappaB signal transduction pathways. TAK1, a MAPKKK, is critical for both IL-1- and TNF-induced activation of the NF-kappaB pathway. TAB2, a TAK1-binding protein, is involved in IL-1-induced NF-kappaB activation by physically linking TAK1 to TRAF6. However, IL-1-induced activation of NF-kappaB is not impaired in TAB2-deficient embryonic fibroblasts. Here we report the identification and characterization of a novel protein designated TAB3, a TAB2-like molecule that associates with TAK1 and can activate NF-kappaB similar to TAB2. Endogenous TAB3 interacts with TRAF6 and TRAF2 in an IL-1- and a TNF-dependent manner, respectively. Further more, IL-1 signaling leads to the ubiquitination of TAB2 and TAB3 through TRAF6. Cotransfection of siRNAs directed against both TAB2 and TAB3 inhibit both IL-1- and TNF-induced activation of TAK1 and NF-kappaB. These results suggest that TAB2 and TAB3 function redundantly as mediators of TAK1 activation in IL-1 and TNF signal transduction.
- リンク情報
- ID情報
-
- DOI : 10.1093/emboj/cdg605
- ISSN : 0261-4189
- Web of Science ID : WOS:000187221700011