| First Author | Kim JH | Year | 2019 |
| Journal | Cell Rep | Volume | 27 |
| Issue | 7 | Pages | 2105-2118.e5 |
| PubMed ID | 31091449 | Mgi Jnum | J:288627 |
| Mgi Id | MGI:6432300 | Doi | 10.1016/j.celrep.2019.04.071 |
| Citation | Kim JH, et al. (2019) Small Heterodimer Partner Controls the Virus-Mediated Antiviral Immune Response by Targeting CREB-Binding Protein in the Nucleus. Cell Rep 27(7):2105-2118.e5 |
| abstractText | Small heterodimer partner (SHP) is an orphan nuclear receptor that acts as a transcriptional co-repressor by interacting with nuclear receptors and transcription factors. Although SHP plays a negative regulatory function in various signaling pathways, its role in virus infection has not been studied. Here, we report that SHP is a potent negative regulator of the virus-mediated type I IFN signaling that maintains homeostasis within the antiviral innate immune system. Upon virus infection, SHP interacts specifically with CREB-binding protein (CBP) in the nucleus, thereby obstructing CBP/beta-catenin interaction competitively. Consequently, SHP-deficient cells enhance antiviral responses, including transcription of the type I IFN gene, upon virus infection. Furthermore, SHP-deficient mice show higher levels of IFN production and are more resistant to influenza A virus infection. Our results suggest that SHP is a nuclear regulator that blocks transcription of the type I IFN gene to inhibit excessive innate immune responses. |
