Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q Exactive HF
ORGANISM(S): Homo Sapiens (human) Mus Musculus (mouse)
TISSUE(S): Epithelial Cell, Cell Culture, Fibroblast
DISEASE(S): Influenza
SUBMITTER: Xianghui Kong
LAB HEAD: Zhijian Cai
PROVIDER: PXD039071 | Pride | 2023-01-30
REPOSITORIES: Pride
Action | DRS | |||
---|---|---|---|---|
IP_RIGI_in_HEK293T.raw | Raw | |||
IP_RIGI_in_HEK293T.xlsx | Xlsx | |||
IP_RIGI_in_NIH_3T3.raw | Raw | |||
IP_RIGI_in_NIH_3T3.xlsx | Xlsx | |||
IP_UBE2M_in_NIH_3T3.raw | Raw |
Items per page: 5 1 - 5 of 7 |
Kong Xianghui X Lu Xinliang X Wang Shibo S Hao Jiayue J Guo Danfeng D Wu Hao H Jiang Yu Y Sun Yi Y Wang Jianli J Zhang Gensheng G Cai Zhijian Z
Cell reports 20230119 1
Type I interferon (IFN-I) signaling is central to inducing antiviral innate immunity. However, the mechanisms for IFN-I signaling self-regulation are still largely unknown. Here, we report that RNA virus-infected macrophages with UBE2M deficiency produced decreased IFN-I expression in a RIG-I-dependent manner, causing an aggravated viral infection. Mechanistically, UBE2M inhibits RIG-I degradation by preventing the interaction of RIG-I and E3 ligase STUB1, resulting in antiviral IFN-I signaling ...[more]