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study identifies the AIM2 (zeige AIM2 ELISA Kits) inflammasome and cGAS/IFI16-STING-type I IFN pathway as a novel mechanism for host innate immunity to the ALVAC vaccine vector.
p204 initiated innate antiviral responses in adipose cells, thereby modulating adipocyte function.
cGAS and Ifi204 cooperate to produce type I IFNs in response to Francisella infection.
The present study demonstrated that mouse Leydig cells had innate antiviral activities in response to viral DNA challenge through p204 activation.
Data indicate that the transient expression of p204 in the early stage is indispensable for adipocyte differentiation. Disruption of p204 expression patterns at this stage leads to irreversible damage in fat formation.
IFI16 exerts in vivo anti-tumoral activity by promoting apoptosis of tumor cells.
This gene product interacts with the Tpr protein, a component of the nuclear pore complex.
expression of p204 is activated by the cardiac Gata4 (zeige GATA4 ELISA Kits), Nkx2.5 (zeige NKX2-5 ELISA Kits), and Tbx5 (zeige TBX5 ELISA Kits) proteins
binding of Id1, Id2, or Id3 protein to the Gata4 and Nkx2.5 proteins inhibits the p204-induced differentiation of P19 cells to myocytes
p204 synergizes with pRb (zeige PGR ELISA Kits) in the stimulation of Cbfa1 (zeige RUNX2 ELISA Kits)-dependent gene activation and osteoblast differentiation
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
this study shows that IFI16 is not essential for the IFN response to human cytomegalovirus infection
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 (zeige TBK1 ELISA Kits)/IRF3 (zeige IRF3 ELISA Kits) signaling pathway but is required for downstream antiviral cytokine expression.
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.
Findings indicate that expression of the scleroderma autoantigens IFI-16 and CENPs (zeige APITD1 ELISA Kits), 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.
DDR (zeige DDR1 ELISA Kits)-induced signaling in cells activates the ATM (zeige ATM ELISA Kits)-p53 (zeige TP53 ELISA Kits) and ATM (zeige ATM ELISA Kits)-IKKalpha (zeige CHUK ELISA Kits)/beta-interferon (zeige IFNA ELISA Kits) (IFN)-beta (zeige IFNB1 ELISA Kits) signaling pathways, thus leading to an induction of the p53 (zeige TP53 ELISA Kits) and IFN-inducible IFI16 gene
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.
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.
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.
This gene encodes a member of the HIN-200 (hematopoietic interferon-inducible nuclear antigens with 200 amino acid repeats) family of cytokines. The encoded protein contains domains involved in DNA binding, transcriptional regulation, and protein-protein interactions. The protein localizes to the nucleoplasm and nucleoli, and interacts with p53 and retinoblastoma-1. It modulates p53 function, and inhibits cell growth in the Ras/Raf signaling pathway. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
interferon, gamma-inducible protein 16
, interferon, gamma-inducible gene 204
, interferon-activable protein 204
, interferon-inducible protein p204
, gamma-interferon-inducible protein 16
, interferon-gamma induced protein IFI 16
, interferon-inducible myeloid differentiation transcriptional activator
, interferon activated gene 203
, Gamma-interferon-inducible protein Ifi-16