TRAF-interacting protein with a forkhead-associated domain B (TIFAB) is a negative regulator of the TRAF6-induced cellular functions.

Takayuki Matsumura*, Junko Kawamura-Tsuzuku, Tadashi Yamamoto, Kentaro Semba, Jun Ichiro Inoue

*この研究の対応する著者

研究成果: Article査読

14 被引用数 (Scopus)

抄録

Tumour necrosis factor receptor-associated factor (TRAF)-interacting protein with a forkhead-associated domain (TIFA) activates TRAF6 to induce NF-kappaB activation. TIFA-related protein, TIFAB, is highly expressed in the spleen and inhibits TIFA-mediated TRAF6 activation. However, little is known about cell types that express TIFAB and its function in those cells. Here, we show that TIFAB is mainly expressed in B cells rather than T cells in the spleen and that the expression level was much higher in dendritic cells (DCs) and macrophages than that in splenic lymphocytes. TIFAB expression was downregulated when B cells, DCs or macrophages were stimulated by TRAF6-mediated proliferative or maturation signals including those emanating from CD40, sIgM and TLRs. Furthermore, microinjection experiments using NIH3T3 cells revealed that TIFAB inhibited entry into the S phase of the cell cycle. Our results suggest that TIFAB could act as a negative regulator of the TRAF6-induced cellular function such as B cell proliferation and maturation of DCs and macrophages.

本文言語English
ページ(範囲)375-381
ページ数7
ジャーナルJournal of biochemistry
146
3
DOI
出版ステータスPublished - 2009 9月

ASJC Scopus subject areas

  • 生化学
  • 分子生物学

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