2022 Fiscal Year Annual Research Report
| Project/Area Number |
21J14073
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| Research Institution | The University of Tokyo |
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Principal Investigator |
趙 東儀 東京大学, 薬学系研究科, 特別研究員(DC2)
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| Project Period (FY) |
2021-04-28 – 2023-03-31
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| Keywords | Type I IFN / Apoptosis / MAVS |
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| Outline of Annual Research Achievements |
Host cells activate the first line of defense mechanisms, such as apoptosis or induction of type I interferon (IFN), to prevent virus replication and proliferation upon virus infection. RIG-I-like receptors (RLRs) recognize single-stranded RNA (ssRNA) or double-stranded RNA (dsRNA) of viruses, and bind with Mitochondrial antiviral signaling (MAVS) to induce these defense responses. Among the MAP3Ks mediating the innate immune response to viruses via MAVS, ASK1 is particularly important. Previous studies have discovered that Apoptosis Signal Regulating Kinase 1 (ASK1) promotes the expression of type I IFN in response to virus infection. However, it was unclear how ASK1 controls type I IFN production.
Our research revealed that ASK1 promotes the phosphorylation of MAVS. In MEFs expressing a MAVS phosphorylation-defective mutant, the production of type I IFN was suppressed and the replication of Sendai virus was promoted upon virus infection. These results suggest that the phosphorylation of MAVS mediated by ASK1 is necessary for protection against virus infection.
In summary, our research suggests that the phosphorylation of MAVS mediated by ASK1 is necessary for the protection of host cells against virus infection.
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| Research Progress Status |
令和4年度が最終年度であるため、記入しない。
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| Strategy for Future Research Activity |
令和4年度が最終年度であるため、記入しない。
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