BS69 cooperates with TRAF3 in the regulation of Epstein–Barr virus-derived LMP1/CTAR1-induced NF-κB activation

• Ikeda, Osamu

• Miyasaka, Yuto

• Yoshida, Ryuji

• Mizushima, Akihiro

• Oritani, Kenji

• Sekine, Yuichi

• Kuroda, Makoto

• Yasui, Teruhito

• Fujimuro, Masahiro

• Muromoto, Ryuta

• Nanbo, Asuka

• Matsuda, Tadashi

書誌事項

タイトル別名

• Physical and functional interactions between BS69 and LMP1/CTAR1

抄録

Epstein-Barr virus latent membrane protein 1 (LMP1) activates NF-κB signaling pathways through two C-terminal regions, CTAR1 and CTAR2. Previous studies have demonstrated that BS69, a multidomain cellular protein, regulates LMP1/CTAR2-mediated NF-κB activation by interfering with the complex formation between TRADD and LMP1/CTAR2. Here, we found that BS69 directly interacted with the LMP1/CTAR1 domain and regulated LMP1/CTAR1-mediated NF-κB activation and subsequent IL-6 production. Regarding the mechanisms involved, we found that BS69 directly interacted with TRAF3, a negative regulator of NF-κB activation. Furthermore, small-interfering RNA-mediated knockdown experiments revealed that TRAF3 was involved in the BS69-mediated suppression of LMP1/CTAR1-induced NF-κB activation.

収録刊行物

• FEBS Letters

  FEBS Letters 584 (5), 865-872, 2010-03-05

  Elsevier

キーワード

• BS69
• EBV
• LMP1
• TRAF3
• NF-κB
• transcription

詳細情報

• CRID: 1050845763935853952
• NII論文ID: 120001875432
• NII書誌ID: AA00642943
• HANDLE: 2115/42639
• ISSN: 00145793
• 本文言語コード: en
• 資料種別: journal article
• データソース種別:
  • IRDB
  • CiNii Articles