Sandbox GGC12: Difference between revisions

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IRF3

Transcriptional regulator of type I interferon (IFN)-dependent immune responses which plays a critical role in the innate immune response against DNA and RNA viruses. ~~Regulates~~ the transcription of type I IFN genes (IFN-alpha and IFN-beta) and IFN-stimulated genes (ISG) by binding to an interferon-stimulated response element (ISRE) in their promoters. ~~Acts~~ as a more potent activator of the IFN-beta (IFNB) gene than the IFN-alpha (IFNA) gene and plays a critical role in both the early and late phases of the IFNA/B gene induction. ~~Found~~ in an inactive form in the cytoplasm of uninfected cells and following viral infection, double-stranded RNA (dsRNA), or toll-like receptor (TLR) signaling, is phosphorylated by IKBKE and TBK1 kinases. ~~This induces~~ a conformational change, leading to its dimerization and nuclear localization and association with CREB binding protein (CREBBP) to form dsRNA-activated factor 1 (DRAF1), a complex which activates the transcription of the type I IFN and ISG genes. Can activate distinct gene expression programs in macrophages and can induce significant apoptosis in primary macrophages <ref>DOI 10.1038/nri3581</ref> <ref>DOI 10.1016/j.coviro.2011.11.001</ref>.

Transcriptional regulator of type I interferon (IFN)-dependent immune responses which plays a critical role with the innate immune response against DNA and RNA viruses. It will occssionally regulate the transcription of type I IFN genes (IFN-alpha and IFN-beta) and IFN-stimulated genes (ISG) by binding to an interferon-stimulated response element (ISRE) with their promoters. It would act as a more potent activator of the IFN-beta (IFNB) gene than the IFN-alpha (IFNA) gene and plays a critical and significant role in both the early and late phases of the IFNA/B gene induction. There are going to be found in an inactive form within the cytoplasm of uninfected cells and following the viral infection, double-stranded RNA (dsRNA), or toll-like receptor (TLR) signaling, is going to be phosphorylated by IKBKE and TBK1 kinases. There are going to induce a conformational change, leading to its dimerization and nuclear localization and association with CREB binding protein (CREBBP) to form dsRNA-activated factor 1 (DRAF1), a complex which activates the transcription of the type I IFN and ISG genes. Can activate distinct gene expression programs in macrophages and can induce significant apoptosis in primary macrophages <ref>DOI 10.1038/nri3581</ref> <ref>DOI 10.1016/j.coviro.2011.11.001</ref>.

== Structural highlights ==

Sandbox GGC12: Difference between revisions

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 IRF3
-Transcriptional regulator of type I interferon (IFN)-dependent immune responses which plays a critical role in the innate immune response against DNA and RNA viruses. Regulates the transcription of type I IFN genes (IFN-alpha and IFN-beta) and IFN-stimulated genes (ISG) by binding to an interferon-stimulated response element (ISRE) in their promoters. Acts as a more potent activator of the IFN-beta (IFNB) gene than the IFN-alpha (IFNA) gene and plays a critical role in both the early and late phases of the IFNA/B gene induction. Found in an inactive form in the cytoplasm of uninfected cells and following viral infection, double-stranded RNA (dsRNA), or toll-like receptor (TLR) signaling, is phosphorylated by IKBKE and TBK1 kinases. This induces a conformational change, leading to its dimerization and nuclear localization and association with CREB binding protein (CREBBP) to form dsRNA-activated factor 1 (DRAF1), a complex which activates the transcription of the type I IFN and ISG genes. Can activate distinct gene expression programs in macrophages and can induce significant apoptosis in primary macrophages <ref>DOI 10.1038/nri3581</ref> <ref>DOI 10.1016/j.coviro.2011.11.001</ref>.
+Transcriptional regulator of type I interferon (IFN)-dependent immune responses which plays a critical role with the innate immune response against DNA and RNA viruses. It will occssionally regulate the transcription of type I IFN genes (IFN-alpha and IFN-beta) and IFN-stimulated genes (ISG) by binding to an interferon-stimulated response element (ISRE) with their promoters.  It would act as a more potent activator of the IFN-beta (IFNB) gene than the IFN-alpha (IFNA) gene and plays a critical and significant role in both the early and late phases of the IFNA/B gene induction. There are going to be found in an inactive form within the cytoplasm of uninfected cells and following the viral infection, double-stranded RNA (dsRNA), or toll-like receptor (TLR) signaling, is going to be phosphorylated by IKBKE and TBK1 kinases. There are going to induce a conformational change, leading to its dimerization and nuclear localization and association with CREB binding protein (CREBBP) to form dsRNA-activated factor 1 (DRAF1), a complex which activates the transcription of the type I IFN and ISG genes. Can activate distinct gene expression programs in macrophages and can induce significant apoptosis in primary macrophages <ref>DOI 10.1038/nri3581</ref> <ref>DOI 10.1016/j.coviro.2011.11.001</ref>.
 == Structural highlights ==