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Ifi202b and IFI16 have roles as obesity genes
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In humans with acute and chronic Hepatitis B exists activation of the AIM2 and IFI16 (in acute Hepatitis B), and the activation of the AIM2 and IFI16 can be inhibited by hepatitis B e antigen in chronic Hepatitis B.
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Results suggest that interferon-gamma inducible factor 16 (IFI16) is essential for efficient sensing and signalling upon DNA challenge in macrophages to promote interferons and antiviral responses.
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Data show that both cyclic GMP-AMP synthase (cGAS) and interferon-gamma inducible protein 16 (IFI16) are required for the activation of membrane protein STING (STING) and an innate immune response to exogenous DNA and DNA viruses.
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Interferon-gamma induced protein IFI16 is a unique host factor protein involved in the EBV lifecycle. Reduction of IFI16 protein levels following lytic cycle induction, as well as reactivation from latency after IFI16 mRNA knockdown suggests that IFI16 is crucial for the maintenance of EBV latency.
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This study found IFI16 and AIM2 SNPs associated with higher levels of periodontal microorganisms and an increased percentage of periodontal disease clinical parameters.
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Importantly, knocking down p204, which is reported as the mouse orthologous of human IFI16, inhibited epidermal hyperplasia in mice with imiquimod-induced psoriasiform dermatitis. These findings indicate that IFI16 plays a critical role in the pathogenesis of psoriasis and may be a potential therapeutic target
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IFI16 is a tumour suppressor in HCC via activation of p53 signals and inflammasome
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in a cohort of patients with genital herpes and healthy controls, the minor G allele of the IFI16 single nucleotide polymorphism rs2276404 was associated with resistance to infection
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study identifies the AIM2 inflammasome and cGAS/IFI16-STING-type I IFN pathway as a novel mechanism for host innate immunity to the ALVAC vaccine vector.
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this study shows that IFI16 is not essential for the IFN response to human cytomegalovirus infection
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findings show that IFI16 rapidly oligomerizes at incoming herpesvirus genomes at the nuclear periphery to transcriptionally repress viral gene expression and limit viral replicative capacity; further demonstrate that IFI16 does not initiate upstream activation of the canonical STING/TBK-1/IRF3 signaling pathway but is required for downstream antiviral cytokine expression.
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The authors observed that a reduced IFI16 expression was associated with a very poor survival in chronic lymphocytic leukemia, but only in cases with ZAP70/CD38 expression.
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Findings indicate that expression of the scleroderma autoantigens IFI-16 and CENPs, which are associated with severe vascular disease, is increased in vascular progenitors and mature endothelial cells. High level, lineage-enriched expression of autoantigens may explain the striking association between clinical phenotypes and the immune targeting of specific autoantigens.
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DDR-induced signaling in cells activates the ATM-p53 and ATM-IKKalpha/beta-interferon (IFN)-beta signaling pathways, thus leading to an induction of the p53 and IFN-inducible IFI16 gene
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These studies identify H2B as an innate nuclear sensor mediating a novel extra chromosomal function, and reveal that two IFI16 complexes mediate KSHV and HSV-1 genome recognition responses, with recognition by the IFI16-BRCA1-H2B complex resulting in IFN-beta responses and recognition by IFI16-BRCA1 resulting in inflammasome responses.
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Overall, these data identify a novel activity of the pUL83/IFI16 interactome involved in the regulation of UL54 gene expression and IFI16 stability during early and late phases of human cytomegalovirus replication.
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Together, these results demonstrate that herpes simplex virus 1 promotes the loss of IFI16 through at least two mechanisms: (i) by ICP0-dependent degradation of IFI16 and (ii) by vhs-dependent turnover of IFI16 mRNA.
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These results reveal that Kaposi's sarcoma-associated herpesvirus utilizes the innate immune nuclear DNA sensor IFI16 to maintain its latency and repression of lytic transcripts, and a late lytic Kaposi's sarcoma-associated herpesvirus gene product(s) targets IFI16 for degradation during lytic reactivation.
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Data show that NOD-like receptor signaling genes NOD2, PYCARD, CARD6, and IFI16 are upregulated in psoriatic epidermis.
