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ID 30789
本文ファイル
著者
Nakayama, Keiko
Kato, Tomohisa, Jr
Karin, Michael
キーワード
SIGNALING
CELLCYCLE
PROTEINS
NDC
生物科学・一般生物学
抄録(英)
Proinflammatory cytokines activate NF-κB using the IκB kinase (IKK) complex that phosphorylates inhibitory proteins (IκBs) at N-terminal sites resulting in their ubiquitination and degradation in the cytoplasm. Although ultraviolet (UV) irradiation does not lead to IKK activity, it activates NF-κB by an unknown mechanism through IκBα degradation without N-terminal phosphorylation. Here, we describe an adaptor function of nuclear IKKβ in UV-induced IκBα degradation. UV irradiation induces the nuclear translocation of IκBα and association with IKKβ, which constitutively interacts with β-TrCP through heterogeneous ribonucleoprotein-U (hnRNP-U) leading to IκBα ubiquitination and degradation. Furthermore, casein kinase 2 (CK2) and p38 associate with IKKβ and promote IκBα degradation by phosphorylation at C-terminal sites. Thus, nuclear IKKβ acts as an adaptor protein for IκBα degradation in UV-induced NF-κB activation. NF-κB activated by the nuclear IKKβ adaptor protein suppresses anti-apoptotic gene expression and promotes UV-induced cell death.
掲載誌名
Molecular Cell
39巻
4号
開始ページ
570
終了ページ
582
出版年月日
2010-08-27
出版者
Cell Press
ISSN
1097-2765
NCID
出版者DOI
言語
英語
NII資源タイプ
学術雑誌論文
広大資料タイプ
学術雑誌論文
DCMIタイプ
text
フォーマット
application/pdf
著者版フラグ
author
権利情報
Copyright (c) 2010 Elsevier Inc.
関連情報URL
部局名
医歯薬学総合研究科