Ask about this productRelated genes to: IRF3 protein
- Gene:
- IRF3 NIH gene
- Name:
- interferon regulatory factor 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-13
- Date modifiied:
- 2017-07-07
Related products to: IRF3 protein
Related articles to: IRF3 protein
- Type I interferon (IFN-I) signaling is crucial for antiviral innate immunity. F-box protein-mediated ubiquitination regulates this pathway. FBXO11 positively regulates IFN-I signaling via TRAF3 K63-linked ubiquitination, but whether other F-box proteins act synergistically during HBV infection remains unknown. This study investigates FBXO32 expression and function in HBV infection, and whether FBXO11 and FBXO32 synergistically activate innate immunity through a NEDD8-dependent mechanism. - Source: PubMed
Publication date: 2026/09/03
Li LiqiangTao ShunZhang YunfeiZeng ZihanLi LiangZhang Jun - Klebsiella pneumoniae (K. pneumoniae) liver abscess (KPLA) is frequently accompanied by thrombophlebitis and systemic inflammation. Argatroban, a direct thrombin inhibitor, has anti-inflammatory potential, but its efficacy and mechanism in KPLA remain unclear. - Source: PubMed
Publication date: 2026/09/17
Wang HongguangChen LuluWang HairuiChang Zhihui - Cytosolic DNA sensing through the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) axis is an important component of innate host defense, whereas sustained pathway activation has been implicated in inflammatory and autoimmune diseases. Although several potent STING inhibitors are in preclinical development and ASP5502 has entered clinical evaluation, no STING inhibitor has received regulatory approval. Screening of an FDA-approved compound library identified vitamin K3 (VK3; menadione), a synthetic vitamin K analogue, as a compound that attenuated cellular responses elicited by SR717 and 2'3'-cGAMP. VK3 reduced IRF3 phosphorylation and the expression of interferon-related and inflammatory genes. In a cellular thermal shift assay (CETSA), VK3 did not produce detectable thermal stabilization of STING; therefore, its direct molecular target remains undefined. VK3 did not significantly reduce short-term THP-1 cell viability at the concentration used for signaling experiments. In LPS-challenged THP-1 cells, VK3 attenuated the induction of selected inflammatory transcripts, indicating that effects beyond STING-agonist-stimulated signaling cannot be excluded. In mice, topical VK3 attenuated imiquimod (IMQ)-induced psoriasis-like skin inflammation, reduced IL-17 and IL-23 expression, and did not appreciably affect body weight or the measured organ indices. Among the vitamin K analogues examined, VK3 showed the most consistent attenuation of STING-agonist-induced signaling. These findings support further investigation of VK3 as a topical modulator of inflammatory signaling in skin disease. - Source: PubMed
Publication date: 2026/09/16
Jin ZuyiHuang ZhenZhang YiqinMeng MeichenHong LiangLi Min - 6PPD-quinone (6PPD-Q), a tire rubber-derived contaminant, has raised concern because of its widespread occurrence and potential systemic toxicity. Here, we examined splenic injury and associated innate immune signaling changes after repeated oral 6PPD-Q exposure. Male C57BL/6 mice received 60 μg/kg/day 6PPD-Q by oral gavage for 42 days. Exposure was associated with a reduced spleen index and histopathological disruption, together with increased MDA and 8-OHdG and altered antioxidant indices. qPCR targeting D-loop, CYTB, ND1, and ND4 showed reduced relative mtDNA abundance; these measurements do not directly establish structural mtDNA damage or cytosolic mtDNA release. Concurrently, cGAS-STING-related protein changes and increased phosphorylation ratios of STING, TBK1, and IRF3 were observed, accompanied by NF-κB-related signaling changes. NLRP3-, ASC-, GSDMD-, and inflammatory cytokine-related markers also changed, consistent with altered NLRP3- and pyroptosis-associated signaling. Because cytosolic mtDNA, pathway-specific intervention, and direct pyroptotic cell-death endpoints were not assessed, the observed molecular changes are interpreted as associations rather than evidence of a causal mtDNA-cGAS-STING-pyroptosis axis. These findings identify the spleen as a potential target of repeated 6PPD-Q exposure and provide evidence of splenic injury associated with altered redox status, reduced mtDNA abundance, and innate immune signaling changes. - Source: PubMed
Publication date: 2026/09/16
Zhang YuyiFu LinlinZhang ShuqiBai JiaweiLi XinruJiang XiaowenYu Wenhui - Crosstalk between the nervous and immune systems is responsible for ischemic cerebral injury. However, the molecular mechanism and regulatory network underlying this interaction still have not been completely illuminated. In this study, we found that the E3 SUMOylase Tripartite Motif-Containing Protein 28 (TRIM28) was primarily upregulated in astrocytes after ischemic stroke (IS), and elevated plasma TRIM28 levels correlated with poor prognosis in IS patients. Astrocyte-specific Trim28 knockout relieved IS-mediated cerebral injury. Conversely, in astrocyte-specific Trim28 knockout mice, AAV-mediated re-expression of TRIM28 in astrocytes aggravated IS-mediated neuroinflammation and cerebral injury. Mechanistically, TRIM28 catalyzed SUMO1 conjugation of interferon regulatory factor 3 (IRF3) at lysine 77, which stabilized intranuclear IRF3 by inhibiting K48-linked ubiquitination and subsequent proteasomal degradation. Stabilized IRF3 transcriptionally upregulated C-X-C motif chemokine ligand 1 (CXCL1), thereby enhancing CXCL1-CXCR2 signaling to promote CXCR2 neutrophils chemotaxis and infiltration into the ischemic brain. Importantly, virtual screening of the FDA-approved drug library identified Acarbose as a pharmacological inhibitor of TRIM28-IRF3 axis, and Acarbose administration relieved neutrophils brain infiltration and cerebral injury after IS. Our findings highlight the critical role of TRIM28 in regulating crosstalk between astrocytes and neutrophils and nominate TRIM28 as a tractable therapeutic target for ischemic cerebral injury. - Source: PubMed
Publication date: 2026/09/15
Shu HongxinLuo QinghuaHu PingXu YutianZhu WenpingYang LiLei KunjianLuo MingZhang SiZhu XinyiLiao QiuyeChen ZhihaoZeng QinglinZhu XingenZhu ZijingYan Tengfeng