USP18 positively regulates innate antiviral immunity by promoting K63-linked polyubiquitination of MAVS.
USP18 positively regulates innate antiviral immunity by promoting K63-linked polyubiquitination of MAVS.
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USP18 通过促进 MAVS 的 K63 连接多聚泛素化积极调节先天抗病毒免疫
DOI:
10.1038/s41467-021-23219-4
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发表时间:
2021-05-20
影响因子:
16.6
通讯作者:
Gao C
中科院分区:
文献类型:
--
作者:
Hou J;Han L;Zhao Z;Liu H;Zhang L;Ma C;Yi F;Liu B;Zheng Y;Gao C
Activation of MAVS, an adaptor molecule in Rig-I-like receptor (RLR) signaling, is indispensable for antiviral immunity, yet the molecular mechanisms modulating MAVS activation are not completely understood. Ubiquitination has a central function in regulating the activity of MAVS. Here, we demonstrate that a mitochondria-localized deubiquitinase USP18 specifically interacts with MAVS, promotes K63-linked polyubiquitination and subsequent aggregation of MAVS. USP18 upregulates the expression and production of type I interferon following infection with Sendai virus (SeV) or Encephalomyocarditis virus (EMCV). Mice with a deficiency of USP18 are more susceptible to RNA virus infection. USP18 functions as a scaffold protein to facilitate the re-localization of TRIM31 and enhances the interaction between TRIM31 and MAVS in mitochondria. Our results indicate that USP18 functions as a post-translational modulator of MAVS-mediated antiviral signaling.
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DOI:
10.1084/jem.20151529
发表时间:
2016-06-27
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Meuwissen ME;Schot R;Buta S;Oudesluijs G;Tinschert S;Speer SD;Li Z;van Unen L;Heijsman D;Goldmann T;Lequin MH;Kros JM;Stam W;Hermann M;Willemsen R;Brouwer RW;Van IJcken WF;Martin-Fernandez M;de Coo I;Dudink J;de Vries FA;Bertoli Avella A;Prinz M;Crow YJ;Verheijen FW;Pellegrini S;Bogunovic D;Mancini GM
通讯作者:
Mancini GM
影响因子:
30.3
作者:
Dai, Tong;Wu, Liming;Zhang, Long
通讯作者:
Zhang, Long
影响因子:
158.5
作者:
Alsohime, Fahad;Martin-Fernandez, Marta;Alangari, Abdullah A.
通讯作者:
Alangari, Abdullah A.
影响因子:
4.4
作者:
Kim, KI;Malakhova, OA;Zhang, DE
通讯作者:
Zhang, DE
影响因子:
16.6
作者:
Qi N;Shi Y;Zhang R;Zhu W;Yuan B;Li X;Wang C;Zhang X;Hou F
通讯作者:
Hou F