Ring finger protein 166 potentiates RNA virus-induced interferon-β production via enhancing the ubiquitination of TRAF3 and TRAF6

Hai Wei Chen; Yong Kang Yang; Hao Xu; Wei Wei Yang; Zhong He Zhai; Dan Ying Chen

doi:10.1038/srep14770

Ring finger protein 166 potentiates RNA virus-induced interferon-β production via enhancing the ubiquitination of TRAF3 and TRAF6

Hai Wei Chen
, Yong Kang Yang
, Hao Xu
, Wei Wei Yang
, Zhong He Zhai
, Dan Ying Chen

Research output: Contribution to journal › Article › peer-review

Abstract

Host cells orchestrate the production of IFN-β upon detecting invading viral pathogens. Here, we report that Ring finger protein 166 (RNF166) potentiates RNA virus-triggered IFN-β production. Overexpression of RNF166 rather than its homologous proteins RNF114, RNF125, and RNF138, enhanced Sendai virus (SeV)-induced activation of the IFN-β promoter. Knockdown of endogenous RNF166, but not other RNFs, inhibited the IFN-β production induced by SeV and encephalomyocarditis virus. RNF166 interacted with TRAF3 and TRAF6. SeV-induced ubiquitination of TRAF3 and TRAF6 was suppressed when endogenous RNF166 rather than RNF114/138 was knocked down. These findings suggest that RNF166 positively regulates RNA virus-triggered IFN-β production by enhancing the ubiquitination of TRAF3 and TRAF6.

Original language	English (US)
Article number	14770
Journal	Scientific reports
Volume	5
DOIs	https://doi.org/10.1038/srep14770
State	Published - Oct 12 2015
Externally published	Yes

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@article{f825049dec0d4c018ca3d628cf9fbafd,

title = "Ring finger protein 166 potentiates RNA virus-induced interferon-β production via enhancing the ubiquitination of TRAF3 and TRAF6",

abstract = "Host cells orchestrate the production of IFN-β upon detecting invading viral pathogens. Here, we report that Ring finger protein 166 (RNF166) potentiates RNA virus-triggered IFN-β production. Overexpression of RNF166 rather than its homologous proteins RNF114, RNF125, and RNF138, enhanced Sendai virus (SeV)-induced activation of the IFN-β promoter. Knockdown of endogenous RNF166, but not other RNFs, inhibited the IFN-β production induced by SeV and encephalomyocarditis virus. RNF166 interacted with TRAF3 and TRAF6. SeV-induced ubiquitination of TRAF3 and TRAF6 was suppressed when endogenous RNF166 rather than RNF114/138 was knocked down. These findings suggest that RNF166 positively regulates RNA virus-triggered IFN-β production by enhancing the ubiquitination of TRAF3 and TRAF6.",

author = "Chen, \{Hai Wei\} and Yang, \{Yong Kang\} and Hao Xu and Yang, \{Wei Wei\} and Zhai, \{Zhong He\} and Chen, \{Dan Ying\}",

note = "Funding Information: The authors thank the Core Facilities at the School of Life Sciences, Peking University, for assistance with confocal microscopy, and we are grateful to Dr. Xue-Mei Hao and Xiao-Cheng Li for help with capturing images. This work was supported by the National Natural Science Foundation of China (31170822 and 31470841).",

year = "2015",

month = oct,

day = "12",

doi = "10.1038/srep14770",

language = "English (US)",

volume = "5",

journal = "Scientific reports",

issn = "2045-2322",

publisher = "Nature Research",

}

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T1 - Ring finger protein 166 potentiates RNA virus-induced interferon-β production via enhancing the ubiquitination of TRAF3 and TRAF6

AU - Chen, Hai Wei

AU - Yang, Yong Kang

AU - Xu, Hao

AU - Yang, Wei Wei

AU - Zhai, Zhong He

AU - Chen, Dan Ying

N1 - Funding Information: The authors thank the Core Facilities at the School of Life Sciences, Peking University, for assistance with confocal microscopy, and we are grateful to Dr. Xue-Mei Hao and Xiao-Cheng Li for help with capturing images. This work was supported by the National Natural Science Foundation of China (31170822 and 31470841).

PY - 2015/10/12

Y1 - 2015/10/12

N2 - Host cells orchestrate the production of IFN-β upon detecting invading viral pathogens. Here, we report that Ring finger protein 166 (RNF166) potentiates RNA virus-triggered IFN-β production. Overexpression of RNF166 rather than its homologous proteins RNF114, RNF125, and RNF138, enhanced Sendai virus (SeV)-induced activation of the IFN-β promoter. Knockdown of endogenous RNF166, but not other RNFs, inhibited the IFN-β production induced by SeV and encephalomyocarditis virus. RNF166 interacted with TRAF3 and TRAF6. SeV-induced ubiquitination of TRAF3 and TRAF6 was suppressed when endogenous RNF166 rather than RNF114/138 was knocked down. These findings suggest that RNF166 positively regulates RNA virus-triggered IFN-β production by enhancing the ubiquitination of TRAF3 and TRAF6.

AB - Host cells orchestrate the production of IFN-β upon detecting invading viral pathogens. Here, we report that Ring finger protein 166 (RNF166) potentiates RNA virus-triggered IFN-β production. Overexpression of RNF166 rather than its homologous proteins RNF114, RNF125, and RNF138, enhanced Sendai virus (SeV)-induced activation of the IFN-β promoter. Knockdown of endogenous RNF166, but not other RNFs, inhibited the IFN-β production induced by SeV and encephalomyocarditis virus. RNF166 interacted with TRAF3 and TRAF6. SeV-induced ubiquitination of TRAF3 and TRAF6 was suppressed when endogenous RNF166 rather than RNF114/138 was knocked down. These findings suggest that RNF166 positively regulates RNA virus-triggered IFN-β production by enhancing the ubiquitination of TRAF3 and TRAF6.

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DO - 10.1038/srep14770

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SN - 2045-2322

VL - 5

JO - Scientific reports

JF - Scientific reports

M1 - 14770

ER -

Ring finger protein 166 potentiates RNA virus-induced interferon-β production via enhancing the ubiquitination of TRAF3 and TRAF6

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