Open AccessMARCH3 attenuates IL-1β–triggered inflammation by mediating K48-linked polyubiquitination and degradation of IL-1RI
Author(s) -
Heng Lin,
Deng Gao,
MingMing Hu,
Man Zhang,
Xiaoxia Wu,
Lu Feng,
Wenhua Xu,
Qing Yang,
Xuan Zhong,
Jin Wei,
Zhi-Sheng Xu,
Hongxia Zhang,
Ze-Min Song,
Qian Zhou,
Wen Ye,
Ying Liu,
Shu Li,
HongBing Shu
Publication year - 2018
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.1806217115
Subject(s) - inflammation , ubiquitin , degradation (telecommunications) , chemistry , medicine , immunology , computer science , biochemistry , gene , telecommunications
Significance Infection of pathogenic microbes induces the body to produce cytokines, which are mediators of inflammation. IL-1β plays central roles in the initiation of inflammatory and immune responses. In this study, we identified MARCH3 protein, which negatively regulates IL-1β–triggered signaling and inflammatory response by mediating K48-linked polyubiquitination of IL-1RI at lysine 409 and its lysosomal degradation. Our findings reveal a mechanism for how IL-1β–triggered inflammatory response is attenuated by down-regulation of IL-1β receptor.
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