Ask about this productRelated genes to: IRF3 antibody
- 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 antibody
Related articles to: IRF3 antibody
- Aging is a risk factor for neurodegenerative disorders, but the molecular link between neuronal aging and neurodegeneration remains unclear. Huntington's disease (HD) is an inherited neurodegenerative disorder with adult-onset clinical symptoms. Striatal medium spiny neurons (MSNs) are mainly affected in HD, but how aging contributes to MSN degeneration remains uncertain. Using directly converted MSNs from fibroblasts of HD patients (HD-MSNs), we studied age-related pathological features, including neuronal cell death, mutant huntingtin (mHTT) aggregation, and DNA damage in HD. In this study, through transcriptomic analysis of longitudinally aged MSNs and HD-MSNs, we identified four upstream regulators, NFKB1, SOD1, IRF3, and REST, that modulate downstream gene expression in aged MSNs. Among these, knocking down NFKB1 significantly reduced HD pathologies in HD-MSNs, while overexpressing NFKB1 reversed these protective effects. Overall, these results identify NFKB1 as a key age-associated upstream regulator whose downregulation confers neuronal resilience and is a potential therapeutic target in HD. - Source: PubMed
Publication date: 2026/09/04
Oh Young MiBacallao Emily ALee Shin-AeKim JihyunSwinford SamuelSmith Genevieve EBritt BryceAbdalla Shaymaa MadbouliLee Seong Won - Gastric cancer (GC) remains a leading cause of cancer-related mortality, with progression driven largely by the tumor microenvironment (TME). Tumor-associated macrophages (TAMs), the most abundant immune cells in the GC stroma, drive immune evasion, angiogenesis, metastasis, and chemoresistance through polarization toward an M2-like phenotype. - Source: PubMed
Publication date: 2026/08/20
Zhuang XiaodongYang QiangHuang LiangjiuLiu RishengMa TingGuan LiwenZheng Yana - Chronic inflammation-driven gastric precancerous lesions (GPL) are characterized by progressive immune remodeling toward an immunosuppressive state, yet effective chemopreventive agents targeting this process remain scarce. Here, we identify asiatic acid (AA), a natural pentacyclic triterpenoid, as a STING‑binding compound that contributes to reshaping the gastric immune microenvironment and interfering with the Correa cascade. - Source: PubMed
Publication date: 2026/08/20
Li HaotianShen LiLiu JiabaoSu XiaolanMeng ManYang JianqinChen RunhuaYang ChenLiu Yanjun - This study aims to investigate the inhibitory effect of baicalein on cervical cancer driven by persistent human papillomavirus(HPV) infection and clarify its regulatory mechanism on the mitochondrial antiviral signaling protein(MAVS)-interferon regulatory factor 3(IRF3)-interferon-β(IFN-β) signaling pathway, so as to provide experimental evidence for the clinical transformation of baicalein. AutoDock Vina software was used for molecular docking to predict the binding modes and binding energies of baicalein with MAVS and HPV16 E6 proteins. HPV18-positive HeLa cells and HPV16-positive CaSki cells were cultured in vitro. They were divided into the control group and baicalein groups with low dose(10 μmol·L~(-1)) and high dose(40 μmol·L~(-1)). Meanwhile, the silent MAVS cell model was constructed and divided into the negative control small interfering RNA group(siNC) group, MAVS small interfering RNA(siMAVS) group, siNC + baicalein with high dose(H) group, and siMAVS + baicalein-H group. Cell proliferation and apoptosis were detected by colony formation assay, CCK-8 assay, and flow cytometry. The protein expressions of the MAVS-IRF3-IFN-β pathway and HPV16 E6 were detected by Western blot. A nude mouse model bearing CaSki cell xenografts of cervical cancer was established and randomly divided into five groups with six mice in each group: model group, baicalein with low dose(L) group(10 mg·kg~(-1)), baicalein-H group(40 mg·kg~(-1)), siMAVS + baicalein-H group, and siMAVS + model group. Modeling and administration were completed after anesthesia with pentobarbital sodium. Tumor volume was detected every three days; tumor tissues were stripped and weighed at the end of the experiment; the expressions of pathway-related proteins and oncoproteins in tumor tissues were detected by immunohistochemistry. The results show that the binding energies of baicalein with MAVS and HPV16 E6 proteins are-6.65 and-8.82 kcal·mol~(-1), respectively, with good binding activity. In in vitro experiments, baicalein inhibits the proliferation of HeLa and CaSki cells and promotes their apoptosis in a dose-dependent manner, significantly up-regulating the protein expressions of MAVS, p-IRF3/IRF3, and IFN-β, as well as down-regulating the protein expression of HPV16 E6. After MAVS silencing, the in vitro anti-tumor effect and regulatory pathway effect of baicalein are significantly reversed. In in vivo experiments, there are statistically significant differences in tumor volume, tumor weight, and the expression of related proteins among all groups. The tumor volume and weight in the baicalein-L and baicalein-H groups are significantly lower than those in the model group, with the tumor inhibition rates of 47.22% and 73.61%, respectively. The expressions of MAVS, p-IRF3, and IFN-β in tumor tissues are increased, while the expressions of HPV16 E6 and Ki67 proliferation antigen(Ki67) are decreased. After MAVS silencing, the in vivo tumor inhibition rate of baicalein decreases to 22.22%, and its regulatory pathway effect is significantly weakened. In conclusion, baicalein can directly bind to MAVS and HPV16 E6 proteins and exert an anti-cervical cancer effect driven by persistent HPV infection via activating the MAVS-IRF3-IFN-β mitochondrial antiviral signaling pathway and inhibiting the function of HPV16 E6 oncoprotein. MAVS is a key target for baicalein to exert its anti-tumor effect. - Source: PubMed
Chen JinKang Heng-YuanJiang Yu-HanChen Chen-Chen - This paper aims to investigate the tumor-inhibitory effect and underlying mechanism of Guiqi Yiyuan Ointment combined with cisplatin on Lewis lung cancer tumor-bearing mice based on the cyclic GMP-AMP synthase-stimulator of interferon genes(cGAS-STING) signaling pathway. A Lewis lung cancer tumor-bearing mouse model was established, and the successfully modeled mice were randomly divided into a model group, a cisplatin group, a cisplatin + TCM group, an inhibitor group, an inhibitor + TCM group, and a blank group, with 10 mice in each group. Corresponding interventions were administered to mice in each group for two weeks. Routine blood tests were performed to detect the levels of white blood cells(WBC), red blood cells(RBC), and platelets(PLT) in the peripheral blood of mice; the tumor inhibition rate and the organ indices were calculated; hematoxylin-eosin(HE) staining was used to observe the pathological morphology of tumor tissue; flow cytometry was adopted to detect the proportions of CD4~+ and CD8~+ T lymphocytes in the spleen; enzyme-linked immunosorbent assay was employed to measure the contents of interleukin-4(IL-4) and interferon-γ(IFN-γ) in serum; immunohistochemistry was used to detect the expressions of interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) in tumor tissue; immunofluorescence was applied to detect the expression of interferon-β(IFN-β) in tumor tissue; quantitative polymerase chain reaction(Q-PCR) was used to determine the mRNA expressions of cGAS, STING, and TANK-binding kinase 1(TBK1) in tumor tissue; Western blot(WB) was performed to detect the protein expressions of cGAS, STING, TBK1, interferon regulatory factor 3(IRF3), and phosphorylated-interferon regulatory factor 3(p-IRF3) in tumor tissue. The results show that compared with those in the cisplatin group, the levels of the peripheral blood, the tumor inhibition rate, and the organ indices of mice in the cisplatin + TCM group are significantly increased; pathological damages such as a large number of apoptosis and nuclear fragmentation are observed in tumor tissue; the proportions of T lymphocytes are significantly increased; the content of IFN-γ is significantly increased while the content of IL-4 is decreased; the expression of IL-6 is attenuated; the expression of TNF-α and the fluorescent expression of IFN-β are significantly increased; the mRNA expression levels of cGAS, STING, and TBK1 as well as the protein expression levels of cGAS, STING, TBK1, IRF3, and p-IRF3 are significantly up-regulated. In conclusion, Guiqi Yiyuan Ointment may inhibit tumor growth by regulating the expressions of key molecules in the cGAS-STING signaling pathway and promoting the secretion of downstream IFN-β, thereby reversing Th1/Th2 immune imbalance and restoring the anti-tumor immune response. - Source: PubMed
Xue Mei-HaoWang Jun-HaoGuo Qiong-QiongTian PingXu Long-XinLi Jin-TianLiang Jian-QingHu Rong