RNF90 negatively regulates cellular antiviral responses by targeting MITA for degradation
Mediator of IRF3 activation (MITA, also named as STING/ERIS/MPYS/TMEM173), is essential to DNA virus- or cytosolic DNA-triggered innate immune responses. In this study, we demonstrated the negative regulatory role of RING-finger protein (RNF) 90 in innate immune responses targeting MITA. RNF90 promoted K48-linked ubiquitination of MITA and its proteasome-dependent degradation. Overexpression of RNF90 inhibited HSV-1- or cytosolic DNA-induced immune responses whereas RNF90 knockdown had the opposite effects. Moreover, RNF90-deficient bone marrow-derived dendritic cells (BMDCs), bone marrow-derived macrophages (BMMs) and mouse embryonic fibroblasts (MEFs) exhibited increased DNA virus- or cytosolic DNA-triggered signaling and RNF90 deficiency protected mice from DNA virus infection. Taken together, our findings suggested a novel function of RNF90 in innate immunity.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2020 |
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| Erschienen: |
2020 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:16 |
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| Enthalten in: |
PLoS pathogens - 16(2020), 3 vom: 03. März, Seite e1008387 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Yang, Bo [VerfasserIn] |
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| Links: |
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| Themen: |
EC 2.3.2.27 |
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| Anmerkungen: |
Date Completed 22.06.2020 Date Revised 24.11.2020 published: Electronic-eCollection Citation Status MEDLINE |
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| doi: |
10.1371/journal.ppat.1008387 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM307175057 |
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| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Mediator of IRF3 activation (MITA, also named as STING/ERIS/MPYS/TMEM173), is essential to DNA virus- or cytosolic DNA-triggered innate immune responses. In this study, we demonstrated the negative regulatory role of RING-finger protein (RNF) 90 in innate immune responses targeting MITA. RNF90 promoted K48-linked ubiquitination of MITA and its proteasome-dependent degradation. Overexpression of RNF90 inhibited HSV-1- or cytosolic DNA-induced immune responses whereas RNF90 knockdown had the opposite effects. Moreover, RNF90-deficient bone marrow-derived dendritic cells (BMDCs), bone marrow-derived macrophages (BMMs) and mouse embryonic fibroblasts (MEFs) exhibited increased DNA virus- or cytosolic DNA-triggered signaling and RNF90 deficiency protected mice from DNA virus infection. Taken together, our findings suggested a novel function of RNF90 in innate immunity | ||
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| 700 | 1 | |a Liu, Yue |e verfasserin |4 aut | |
| 700 | 1 | |a Cui, Yuhan |e verfasserin |4 aut | |
| 700 | 1 | |a Song, Di |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Ge |e verfasserin |4 aut | |
| 700 | 1 | |a Ma, Shujun |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Yanzi |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Mengmeng |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Fan |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Hui |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Jie |e verfasserin |4 aut | |
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