| First Author | Jiang W | Year | 2023 |
| Journal | Cell Rep | Volume | 42 |
| Issue | 3 | Pages | 112272 |
| PubMed ID | 36943869 | Mgi Jnum | J:349835 |
| Mgi Id | MGI:7463821 | Doi | 10.1016/j.celrep.2023.112272 |
| Citation | Jiang W, et al. (2023) UBL7 enhances antiviral innate immunity by promoting Lys27-linked polyubiquitination of MAVS. Cell Rep 42(3):112272 |
| abstractText | RNA virus infection usually triggers a range of host immune responses, including the induction of proinflammatory cytokines, interferons, and interferon-stimulated genes (ISGs). Here, we report that UBL7, a ubiquitin-like protein, is upregulated during RNA virus infection and induced by type I interferon as an ISG. UBL7-deficient mice exhibit increased susceptibility to viral infection due to attenuated antiviral innate immunity. UBL7 enhances innate immune response to viral infection by promoting the K27-linked polyubiquitination of MAVS. UBL7 interacts with TRIM21, an E3 ubiquitin ligase of MAVS, and promotes the combination of TRIM21 with MAVS in a dose-dependent manner, facilitating the K27-linked polyubiquitination of MAVS and recruiting of TBK1 to enhance the IFN signaling pathway. Moreover, UBL7 has a broad-spectrum antiviral function as an immunomodulatory adaptor protein. Therefore, UBL7 positively regulates innate antiviral signaling and promotes positive feedback to enhance and amplify the antiviral response. |
