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
- Malathion (MAL) exerts serious reproductive toxicity in males and leads to histopathological injuries in seminiferous tubules, sperm abnormalities, and hormonal disruptions such as reduced testosterone levels. The study assessed whether Lactobacillus acidophilus (L. acidophilus) supplementation could mitigate MAL-induced testicular damage via the crosstalk of cGAS/cGAMP/STING/NF-κB signaling, which in turn modulates the inflammatory cascades IRF3/IFN-β and TNFR/TNF-α, as well as the autophagic markers such as LC3-B/p62. The study also studied the role of miRNA-24 as an upstream regulator. The study included four groups: control, MAL-intoxicated group, L. acidophilus- and scopolamine-treated group. Seminal analysis and histopathological investigations of the testes were done. cGAS, STING, TNFR, IRF3, and miR-24 were estimated using qRT-PCR. cGAMP, IFN-β, LC3-B, and p62 were estimated using ELISA, whereas NF-κB and TNF-α were estimated using immunohistochemical analysis. MAL-intoxicated group showed altered seminal fluid analysis, higher gene expression of cGAS, STING, TNFR, and IRF3, along with lower gene expression of miRNA-24 compared with the control group. Moreover, the concentrations of cGAMP and IFN-β were higher, along with lower concentrations of testosterone, LC3-B, and p62, compared with the control group. Furthermore, NF-κB and TNF-α showed marked positive cytoplasmic expression. However, the L. acidophilus-treated group reversed all the above-mentioned findings. Collectively, the present study showed that MAL-exposure induces testicular toxicity via activating the cGAS/cGAMP/STING/IRF3/NF-κB/TNF-α axis, mediated by miRNA-24. L. acidophilus treatment alleviated these adverse effects, not only by restoring sperm quality, hormonal balance, and tissue architecture but also by suppressing the inflammatory signaling cascade, reactivating autophagic flux, and upregulating protective miRNA-24. - Source: PubMed
Abd-Elmawla Mai AEl Magdoub Hekmat MAboulmagd Yara MEl-Mahdy Safaa MDessouky NesrineAborehab Nora M - Natural products are biologically active compounds used for therapeutic interventions for various diseases, particularly infections. Autophagy is an intracellular catabolic pathway involving lysosomal degradation and is closely associated with immunological pathways, effectively combating bacterial, viral, fungal, and parasitic infections. Accumulating evidence suggests that autophagy activation or inhibition by natural products promotes antimicrobial responses against various pathogens. Numerous natural products can modulate autophagy through diverse signaling pathways, suggesting their potential as a host-directed therapeutic strategy that may complement conventional drug regimens or help mitigate drug resistance in various infectious diseases. However, it remains largely unclear whether these effects are mediated by direct modulation of autophagy or indirectly through associated mechanisms, including enhanced immune defense, attenuation of pathological inflammation, or crosstalk with other organelle functions. Additionally, multiple pathogens can evade host responses; thus, autophagy activation may inadvertently create favorable conditions for certain pathogens. This review discusses the current knowledge of natural products in terms of their antimicrobial actions through autophagy regulation, particularly the roles of distinct natural product classes, such as polyphenols, alkaloids, terpenoids, quinones, peptides, and macrolides in modulating autophagy for potentially contributing to control various infectious diseases. Exploring the intricate molecular interplay between natural products and autophagy in limiting infections may provide valuable insights that could inform the development of innovative host-directed antimicrobial treatments based on autophagy regulation. 3-MA: 3-methyladenine; AM: alveolar macrophages; AMP: antimicrobial peptides; AMPK: 5' adenosine monophosphate-activated protein kinase; ARDS: acute respiratory distress syndrome; ART: artemisinin; ASFV: African swine fever virus; ATG: autophagy related; AZM: azithromycin; BafA1: bafilomycin A; BECN1: beclin 1; BMDM: bone marrow-derived macrophage; BNIP3: BCL2 interacting protein 3; BNIP3L: BCL2 interacting protein 3 like; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CAMKK2: calcium/calmodulin-dependent protein kinase kinase 2; CBD: cannabidiol; CF: cystic fibrosis; CGA: chlorogenic acid; CGAS: cyclic GMP-AMP synthase; CHUK/IKKα: component of inhibitor of nuclear factor kappa B kinase complex; CLP: cecal ligation and puncture; CLR: clarithromycin; CMA: chaperone-mediated autophagy; CoV: coronavirus; DHT: dihydrotanshinone I; EGCG: epigallocatechin-3-gallate; EIF2A: eukaryotic translation initiation factor 2A; EIF2AK2: eukaryotic translation initiation factor 2 alpha kinase 2; ESKAPE: , and spp.; ESRRA: estrogen related receptor alpha; FOXO1: forkhead box O1; FUNDC1: FUN14 domain containing 1; HBV: hepatitis B virus; HCV: hepatitis C virus; HDT: host-directed therapy; HIV: human immunodeficiency virus; HMGB1: high mobility group box 1; HSV: herpes simplex virus; IAV: influenza A virus; ICT: isocryptotanshinone; IFN: interferon; IKBKB/IKKβ: inhibitor of nuclear factor kappa B kinase subunit beta; IL: interleukin; INH: isoniazid; IRF3: IFN regulatory factor 3; KEAP1: kelch like ECH associated protein 1; LAMP: lysosomal associated membrane protein; LAP: LC3-associated phagocytosis; LPS: lipopolysaccharide; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAPK: mitogen-activated protein kinase; MDM: monocyte-derived macrophage; MDR: multidrug-resistant; MON: monotropein; Mtb: ; MTOR: mechanistic target of rapamycin kinase; mtROS: mitochondrial ROS; NET: neutrophil extracellular trap; NFE2L2/Nrf2: NFE2 like bZIP transcription factor 2; NFKB/NF-κB: nuclear factor kappa B; NLRP3: NLR family pyrin domain containing 3; NLRX1: NLR family member X1; NOTCH1: notch receptor 1; NTM: nontuberculous mycobacteria; OMS: ohmyungsamycin; PAK1: p21 (RAC1) activated kinase 1; PINK1: PTEN induced kinase 1; PKM/PKM2: pyruvate kinase M1/2; PLD: phospholipase D; PM: peritoneal macrophage; PPM1A: protein phosphatase, Mg2+/Mn2+ dependent 1A; PRKN/parkin: parkin RBR E3 ubiquitin protein ligase; PtdIns3K: phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol-3-phosphate; PTEN: phosphatase and tensin homolog; RB1CC1/FIP200: RB1 inducible coiled-coil 1; RELA/p65: RELA proto-oncogene, NF-kB subunit; RIF: rifampicin; ROS: reactive oxygen species; RSV: resveratrol; RUBCN/rubicon: rubicon autophagy regulator; SAR: selective autophagy receptor; SIRT: sirtuin; STING1: stimulator of interferon response cGAMP interactor 1; STX17: syntaxin 17; Tat: trans-activator of transcription; TB: tuberculosis; TBK1: TANK binding kinase 1; TFEB: transcription factor EB; TLR: toll like receptor; TNA: tanshinone IIA; TNF: tumor necrosis factor; UA: ursolic acid; ULK1/Atg1: unc-51 like autophagy activating kinase 1; UPR: unfolded protein response; UVRAG: UV radiation resistance associated; VAMP8: vesicle associated membrane protein 8; VDR: vitamin D receptor; WIPI2: WD repeat domain, phosphoinositide interacting 2; ZFYVE1/DFCP1: zinc finger FYVE-type containing 1; ZIKV: Zika virus. - Source: PubMed
Publication date: 2026/04/28
Paik SeungwhaUm SoohyunKim In SooPark Eun-JinKim Kyung TaeBasu JoyotiOh Dong-ChanJo Eun-Kyeong - - Source: PubMed
Publication date: 2026/04/28
Geng ManmanHe AiliJin QiaoyanLiang DongxiaRen XiaoyuLi XiaomengGuan YanglongZhang ChongyuLu YaqiZhang JingZhang WentaoCheng YuanyuanLi YingnanOuyang YuanshuoChang KeweiMeng LiesuZhu WenhuaLu Shemin - Cervical cancer remains a major global health burden. Conventional surgery, radiotherapy, and chemotherapy are limited by insufficient tumor targeting, severe systemic toxicity, and drug resistance, highlighting an urgent need for safe, precise, and combinatorial therapeutic strategies. In this work, we fabricated one-step self-assembled GE11/RGD dual-ligand-modified copper nanoassemblies (GR@Cu NPs). These nanoparticles display densely modified targeting peptides on a copper-rich surface and enable efficient tumor accumulation with minimal off-target distribution. Under 980 nm near-infrared irradiation (1.0 W/cm, 5 min), GR@Cu NPs trigger a photothermal-copper ion synergistic cascade. The rapid release of Cu promotes dihydrolipoamide S-acetyltransferase oligomerization, ferredoxin 1 (FDX1) downregulation, and mitochondrial collapse, thereby initiating cuproptosis. The leaked mitochondrial DNA (mtDNA) further activates the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING)-interferon regulatory factor 3 (IRF3) pathway, reshaping the antitumor immune microenvironment. In vitro, GR@Cu NPs are rapidly and selectively internalized by HeLa and SiHa cervical cancer cells. In a HeLa xenograft nude mouse model, a single 5 min laser irradiation (1.0 W/cm, tumor temperature ∼ 51 °C) achieves potent and long-lasting tumor suppression for 21 days, without obvious body weight loss or histological damage to major organs. By integrating dual-ligand targeting with synergistic cuproptosis and photothermal therapy, this study provides an effective, low-toxicity, and precise strategy for cervical cancer treatment. - Source: PubMed
Publication date: 2026/04/27
Yang NanLiu LuDing LuChen ZhenSu TianyuanYang ZuolingXu XiaoyaTang LinWei ZhiyiDu JiamingGao ChangXue ShiyunGuo XiaobinFeng YonghaiLi Rong - The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway serves as a central innate immune signaling axis in host defense against DNA virus infections, and RNA viruses have also evolved diverse strategies to counteract this pathway. Encephalomyocarditis virus (EMCV), a zoonotic RNA virus, utilizes its 2C protein to antagonize RIG-I-like receptor-mediated type I interferon signaling and induce autophagic degradation of calcium binding and coiled-coil domain 2, thereby evading host antiviral immunity. However, the precise molecular mechanism by which EMCV 2C protein modulates the cGAS-STING pathway remains incompletely understood. Herein, we show that EMCV infection reduces the expression of cGAS and STING proteins, and its 2C protein significantly suppresses the production of IFN-β triggered by poly(dA:dT) or viral infection, as well as the mRNA expression of interferon-stimulated genes. Mechanistically, 2C protein binds to STING via its ATPase domain and facilitates K48-linked polyubiquitination and proteasomal degradation of STING, while dominantly interfering STING translocation to the Golgi apparatus and the formation of STING-TBK1-IRF3 complex, thereby blocking STING-mediated IFN-β signal transduction at multiple levels. This study reveals a novel mechanism by which the EMCV 2C protein suppresses the host antiviral response by targeting STING and promoting its ubiquitination and degradation. This finding deepens understanding of the immune evasion mechanism of EMCV and provides a theoretical foundation for the development of antiviral therapies targeting the 2C protein of picornaviruses. - Source: PubMed
Publication date: 2026/04/05
Cheng RongrongDong PinganXing WeiJin HongyuanMa TingtingXie JingyingWen YanqiaoSu BixiuLi XiangrongFeng Ruofei