An LRP16-containing preassembly complex contributes to NF-κB activation induced by DNA double-strand breaks.
An LRP16-containing preassembly complex contributes to NF-κB activation induced by DNA double-strand breaks.
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含有 LRP16 的预组装复合物有助于 DNA 双链断裂诱导的 NF-kappa B 激活
DOI：
10.1093/nar/gkv161
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发表时间：
2015-03-31
影响因子：
14.9
通讯作者：
Han W
中科院分区：
文献类型：
--
作者：
Wu Z;Wang C;Bai M;Li X;Mei Q;Li X;Wang Y;Fu X;Luo G;Han W
The activation of NF-κB has emerged as an important mechanism for the modulation of the response to DNA double-strand breaks (DSBs). The concomitant SUMOylation and phosphorylation of IKKγ by PIASy and ATM, respectively, is a key event in this mechanism. However, the mechanism through which mammalian cells are able to accomplish these IKKγ modifications in a timely and lesion-specific manner remains unclear. In this study, we demonstrate that LRP16 constitutively interacts with PARP1 and IKKγ. This interaction is essential for efficient interactions among PARP1, IKKγ, and PIASy, the modifications of IKKγ, and the activation of NF-κB following DSB induction. The regulation of LRP16 in NF-κB activation is dependent on the DSB-specific sensors Ku70/Ku80. These data strongly suggest that LRP16, through its constitutive interactions with PARP1 and IKKγ, functions to facilitate the lesion-specific recruitment of PARP1 and IKKγ and, ultimately, the concomitant recruitment of PIASy to IKKγ in response to DSB damage. Therefore, the study has provided important new mechanistic insights concerning DSB-induced NF-κB activation.
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影响因子：
16
作者：
Krishnakumar R;Kraus WL
通讯作者：
Kraus WL
长非编码 RNA HOTAIR 是恶性肿瘤的驱动因素，可预测食管鳞状细胞癌的阴性预后并表现出致癌活性
影响因子：
8.8
作者：
Li, X.;Wu, Z.;Mei, Q.;Li, X.;Guo, M.;Fu, X.;Han, W.
通讯作者：
Han, W.
影响因子：
30.8
作者：
Khanna, KK;Jackson, SP
通讯作者：
Jackson, SP
影响因子：
4.8
作者：
Chen, Dawei;Vollmar, Melanie;Ahel, Ivan
通讯作者：
Ahel, Ivan
影响因子：
7.5
作者：
Gagné, JP;Hendzel, MJ;Poirier, GG
通讯作者：
Poirier, GG