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anti-Human IFI16 Antibodies:
anti-Rat (Rattus) IFI16 Antibodies:
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Human Monoclonal IFI16 Primary Antibody for IHC (p), ELISA - ABIN516822
Anthonio, Brees, Baumgart-Vogt, Hongu, Huybrechts, Van Dijck, Mannaerts, Kanaho, Van Veldhoven, Fransen: Small G proteins in peroxisome biogenesis: the potential involvement of ADP-ribosylation factor 6. in BMC cell biology 2009
Human Polyclonal IFI16 Primary Antibody for ICC, IF - ABIN4321056
Tervaniemi, Katayama, Skoog, Siitonen, Vuola, Nuutila, Sormunen, Johnsson, Linnarsson, Suomela, Kankuri, Kere, Elomaa: NOD-like receptor signaling and inflammasome-related pathways are highlighted in psoriatic epidermis. in Scientific reports 2016
these results showed that HSV-1 infection can enhance the expression of IFI16 in the human term placenta
Enforced expression of IFI16-b inhibits the activation of AIM2 inflammasome, whereas knockdown of IFI16-b augments interleukin-1b secretion triggered by dsDNA but not dsRNA Thus, cytoplasm-localized IFI16-b is functionally equivalent to mouse p202 that exerts an inhibitory effect on AIM2 inflammasome.
data suggest a critical role for IFI16 during HTLV-1 infection by interacting with HTLV-1 RTI ssDNA90 and restricting HTLV-1 replication
The authors propose that IFI16 filaments with associated restriction factors that form in replication compartments constitute a "restrictosome" structure that signals in cis and trans to silence the progeny viral DNA throughout the herpes simplex virus 1-infected cell nucleus.
This non-canonical activation of STING is mediated by the DNA binding protein IFI16, together with the DNA damage response factors ATM and PARP-1.
Ifi202b and IFI16 have roles as obesity genes
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.
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.
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.
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.
This study found IFI16 and AIM2 SNPs associated with higher levels of periodontal microorganisms and an increased percentage of periodontal disease clinical parameters.
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
IFI16 is a tumour suppressor in HCC via activation of p53 signals and inflammasome
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
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.
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/IRF3 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, 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-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
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.
gamma-interferon-inducible protein 16
, interferon-gamma induced protein IFI 16
, interferon-inducible myeloid differentiation transcriptional activator
, interferon, gamma-inducible protein 16
, Gamma-interferon-inducible protein Ifi-16
, interferon induced transmembrane protein 2 (1-8D)
, interferon induced transmembrane protein, like
, interferon-induced transmembrane protein 2
, interferon-inducible protein 16
, interferon activated gene 203
, interferon-activable protein 203
, pyrin and HIN domain-containing protein 1