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Transcriptional response to drug-induced oligomerization of the AIM2-like receptors IFI16, PYHIN1, and MNDA.

ABSTRACT: We explored ALR function in a ligand-independent manner using a drug-inducible dimerization system in which ALRs were tagged with two FV domains that rapidly oligomerize upon addition of the drug AP1 We found that oligomerization of IFI16, PYHIN1, or MNDA did not result in any significant gene expression changes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE80598 | GEO | 2016/05/31

SECONDARY ACCESSION(S): PRJNA319948

REPOSITORIES: GEO

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Transcriptional response to drug-induced oligomerization of the AIM2-like receptors IFI16, PYHIN1, and MNDA.

Project description:We explored ALR function in a ligand-independent manner using a drug-inducible dimerization system in which ALRs were tagged with two FV domains that rapidly oligomerize upon addition of the drug AP1 We found that oligomerization of IFI16, PYHIN1, or MNDA did not result in any significant gene expression changes. Total RNA was isolated from BFP, IFI16-2xFV, PYHIN1-2xFV, or MNDA-2xFV-expressing THP1 cells mock-treated or treated with 30nM AP1 dimerizer drug for 4 or 12 hours.

2016-05-31 | E-GEOD-80598 | biostudies-arrayexpress

Pyrin oligomerization nucleates antiviral IFI16 sensing of herpesvirus DNA

Project description:The formation of multimerized protein assemblies has emerged as a core component of immune signal amplification, yet the biochemical basis of this phenomenon remains unclear for many mammalian proteins within host defense pathways. The interferon-inducible protein 16 (IFI16) is a viral DNA sensor that oligomerizes upon binding to nuclear viral DNA and induces downstream antiviral responses. Here, we first generated oligomerization-incompetent IFI16 mutants that exhibit severely reduced ability to induce antiviral cytokine expression, suppress herpes simplex virus 1 (HSV-1) protein levels, and restrict viral progeny production. Using immunoaffinity purification and targeted mass spectrometry, we establish that oligomerization promotes IFI16 interactions with several proteins involved in transcriptional regulation, including PAF1C, UBTF, and ND10

2019-07-10 | PXD014349 | Pride

Homo sapiens

Project description:Transcriptional response to drug-induced oligomerization of the AIM2-like receptors IFI16, PYHIN1, and MNDA.

| PRJNA319948 | ENA

Transcriptional response to intracellular DNA in cells lacking AIM2-like receptors

Project description:Analysis of ALR-deficient cells indicates that ALRs are not required for the IFN response to intracellular DNA. To explore whether AIM2-like receptors activated another innate signaling pathway upon DNA detection, we performed microarray analysis comparing ALR+/+, ALR-/-, and AIM2-/- macrophages and fibroblasts 4 or 8 hours after transfection with calf-thymus DNA. Total RNA was isolated from ALR+/+, ALR-/-, and AIM2-/- bone marrow-derived macrophages (BMMs) or fibroblasts (MEFs) mock-treated (lipofectamine alone) or transfected with 5ug CT-DNA for 4 or 8 hours.

2016-05-31 | E-GEOD-80766 | biostudies-arrayexpress

Innate immune sensing of influenza virus through IFI16 promote pyroptosis.

Project description:We report that IFI16, which was previously identified as a cytosolic DNA sensor, is essential for the activation of programmed cell death pathways in IAV infected cells. We have identified IFI16 as an innate immune sensor of the influenza A virus. We find that IFI16 recognizes viral genomic RNA upon infection. The activation of IFI16, in turn, triggers the production of type I, III interferons, and also other pro-inflammatory cytokines via the STING-TBK1 and Pro-caspase-1 signalling axis, thereby promoting cell death (apoptosis and pyroptosis in IAV infected cells).

2021-12-31 | GSE163705 | GEO

Transcriptional response to intracellular DNA in cells lacking AIM2-like receptors

2016-05-31 | GSE80766 | GEO

IFI16 functions as an antiviral factor during influenza virus infection by binding viral RNA and enhancing the RIG-I signaling (RNA-seq)

Project description:RIG-I is thought to be the most important sensor of influenza virus infection and plays critical roles in the recognition of cytoplasmic dsRNA and activation of type I IFNs and initiates the innate antiviral immune responses. How the binding of viral RNA to and activation of RIG-I are regulated remains enigmatic. Here, by an affinity proteomics approach with viral RNA as the bait, we found that IFI16, previously identified as a DNA sensor, was significantly induced both in vitro and in vivo during influenza virus infection. Using an IFI16 knockout cells and p204-deficient mice model, we demonstrated that IFI16 enhanced RIG-I-mediated production of type I IFNs and thereby inhibited viral replication during influenza virus infection. Furthermore, we showed that IFI16 regulated the RIG-I signaling by enhancing its transcriptional expression through recruitment of RNA Pol II to the RIG-I promoter. We also verified that IFI16 directly interacted with both viral RNA by HINa domain and associated with RIG-I through its PYRIN domain as well as promoted influenza virus-induced K63-linked polyubiquitination of RIG-I. In addition, we found that IFI16 lost its ability to inhibit viral replication in the absence of RIG-I in virus-infected cells. These results indicate that IFI16 is a key regulator of the RIG-I signaling during antiviral innate immune responses, which highlights a novel mechanism of IFI16 in IAV and other RNA viruses infection, expands our knowledge in antiviral innate immunity, and suggests its possible use as a new strategies to manipulate antiviral responses.

2020-09-09 | GSE157609 | GEO

IFI16 functions as an antiviral factor during influenza virus infection by binding viral RNA and enhancing the RIG-I signaling (RIP-seq)

2020-09-17 | GSE158122 | GEO

IFI16 phase separation via multi-phosphorylation drives innate immune signaling

Project description:Fractionaion of nuclear periphery and core, followed by DDA in primary HFFs at 1 hour post infection with ICP0-RF HSV-1; IP-PRM of IFI16 in primary HFFs at 1 hpi; in vitro kinase assay with IFI16 and select kinases and quantification on phosphorlyated peptides by PRM.

2023-05-22 | PXD034348 | Pride

Inhibition of AIM2 inflammasome activation by a novel transcript isoform of IFI16.

Project description:Mouse p202 is a disease locus for lupus and a dominant-negative inhibitor of AIM2 inflammasome activation. A human homolog of p202 has not been identified so far. Here, we report a novel transcript isoform of human IFI16-designated IFI16-?, which has a domain architecture similar to that of mouse p202. Like p202, IFI16-? contains two HIN domains, but lacks the pyrin domain. IFI16-? is ubiquitously expressed in various human tissues and cells. Its mRNA levels are also elevated in leukocytes of patients with lupus, virus-infected cells, and cells treated with interferon-? or phorbol ester. IFI16-? co-localizes with AIM2 in the cytoplasm, whereas IFI16-? is predominantly found in the nucleus. IFI16-? interacts with AIM2 to impede the formation of a functional AIM2-ASC complex. In addition, IFI16-? sequesters cytoplasmic dsDNA and renders it unavailable for AIM2 sensing. Enforced expression of IFI16-? inhibits the activation of AIM2 inflammasome, whereas knockdown of IFI16-? augments interleukin-1? secretion triggered by dsDNA but not dsRNA Thus, cytoplasm-localized IFI16-? is functionally equivalent to mouse p202 that exerts an inhibitory effect on AIM2 inflammasome.

| S-EPMC6172465 | biostudies-literature

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