IRF1 (C_term)
- Known as:
- IRF1 (C_term)
- Catalog number:
- AP15609PU-S
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- IRF1 (C_term)
Related genes to: IRF1 (C_term)
- Gene:
- IRF1 NIH gene
- Name:
- interferon regulatory factor 1
- Previous symbol:
- -
- Synonyms:
- MAR
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-05-09
- Date modifiied:
- 2016-10-05
Related products to: IRF1 (C_term)
Related articles to: IRF1 (C_term)
- Osteoarthritis (OA) is a leading cause of disability, driven by cartilage degradation, subchondral bone remodeling, and synovial inflammation. Activation of the NF-κB/NLRP3 inflammasome axis contributes to disease progression. This study investigated the chondroprotective and anti-inflammatory effects of intra-articular (IA) metformin (MET) and chlorogenic acid (CGA), alone or in combination, in a rabbit model of OA. OA was induced by monosodium iodoacetate (MIA) injection into the knee joints of male rabbits The rabbits were randomized into six groups: Control, MET + CGA, OA, OA + MET, OA + CGA, and OA + MET + CGA. Disease severity was evaluated via radiography, gross morphology, histopathology, and hematological and synovial fluid analyses. MIA induced OA manifested by joint space narrowing, osteophyte formation, and cartilage erosion, accompanied by elevated serum CRP, increased synovial IL-1β, IL-6, and TNF-α, and upregulation of NF-κB, NLRP3, caspase-1, GSDMD, IRF-1, and cartilage-degrading enzymes. MET or CGA alone significantly attenuated these changes, improving joint architecture, lowering inflammatory cytokines, and suppressing pyroptotic signaling. Combination therapy produced the most pronounced benefits, restoring near-normal cartilage structure, normalizing leukocyte profiles, and reducing molecular markers toward baseline. In silico findings revealed the affinity of CGA to bind with NLRP3 PYD, ASC PYD, IRF-1 and NF-κB p65. In conclusion, IA MET + CGA synergistically ameliorated structural and molecular hallmarks of OA via coordinated inhibition of NF-κB/NLRP3 inflammasome activation and pyroptosis. These findings highlight the translational potential of this dual therapy as a disease-modifying approach for OA management, pending further investigations. - Source: PubMed
Publication date: 2026/06/09
Abdel-Kareem Mona AAbd-Elrafea NourhanAbdo WaliedAtiba Ayman SElsisy Rasha AAlnasser Sulaiman MAlruhaimi Reem SMahmoud Ayman MFarage Amira E - The prioritization of biomarkers that inform molecular-targeted cancer research remains challenging because tumor vulnerabilities are context-dependent. The ubiquitin-proteasome system is essential for cancer cell survival; however, the functional and biomarker-level relevance of individual proteasome subunits has not been systematically defined across cancer types. In this study, we performed an integrative pan-cancer analysis to prioritize proteasome subunits that function as context-dependent vulnerability biomarkers. We analyzed proteasome subunits and proteasome-associated genes across 54 cancer types by integrating large-scale CRISPR ( = 1178 cell lines) and RNAi ( = 707 cell lines) dependency datasets with transcriptomic, survival, immune infiltration, and co-essentiality network analyses. PSMB5 and PSMB6 were prioritized as robust cross-platform and cross-lineage dependency biomarkers, exhibiting reproducible and selective vulnerability patterns across diverse malignancies. Their dependency strength was quantitatively associated with immune-related signaling pathways, including MHC and interferon responses, and inversely correlated with key immune regulatory genes such as NLRC5 and IRF1. Co-essentiality network analysis revealed modular functional organization of proteasome-associated genes, supporting context-dependent roles rather than uniform essentiality. Importantly, the association between proteasome subunits and tumor immune context was externally validated through meta-analysis across 24 independent hepatocellular carcinoma cohorts, demonstrating reproducible correlations with CD4-positive T cell, CD8 T cell, and macrophage infiltration signatures. Functional validation further confirmed that siRNA-mediated knockdown of and significantly impaired proliferation across multiple hepatocellular carcinoma cell lines. Collectively, this study prioritizes PSMB5 and PSMB6 as consistently associated functional biomarkers that integrate genetic dependency and immune context, providing a data-driven framework for stratifying proteasome-targeted therapeutic strategies across cancers. - Source: PubMed
Publication date: 2026/06/04
Kim Jeong HanPark HansolKim Hyo JinHan Myoung-EunLee DongjunYoon SikOh Sae-Ock - Breast cancer is a type of cancer with the highest incidence and mortality rates among women. PD-L1 suppresses the proliferation and activation of T cells, thereby enabling cancer cells to evade immune surveillance and facilitating tumor progression. Micheliolide (MCL) is a guaianolide-type sesquiterpene lactone with broad biological activities. Our results revealed that radiation upregulates PD-L1 expression in breast cancer cells, while MCL pretreatment can inhibit this effect. Bioinformatics analysis combined with shRNA interference experiments confirmed that radiation upregulates PD-L1 by activating the IRF1-STAT1 signaling pathway, while MCL represses PD-L1 transcription by suppressing this pathway. In addition, MCL also downregulates PD-L1 protein level through accelerating proteasomal degradation of PD-L1. In vivo experiments demonstrated that MCL combined with radiotherapy significantly inhibits the growth of syngeneic tumors and increases intratumoral CD8 T cell infiltration and the frequencies of granzyme B-positive cells. Taken together, our results indicate that MCL enhances T-cell-mediated antitumor immunity and improves radiotherapy efficacy through inhibiting IRF1-STAT1 signaling pathway-driven PD-L1 transcription and promoting PD-L1 protein degradation. This study provides a theoretical basis for the clinical application of MCL as an immunomodulator and radiosensitizer. - Source: PubMed
Publication date: 2026/05/25
Peng XuanTan ChunhuaShao YudieLi DandanLi LuKong Peizhong - The interferon regulatory factor (IRF) family serves as pivotal transcriptional regulators that mediate the initiation of host innate immune responses to pathogen invasion by modulating the transcriptional expression of interferon genes, which in turn induces the expression of downstream immune-related genes. However, studies on the IRF gene family in tiger puffer (Takifugu rubripes) remain limited, particularly concerning its functional role in mediating anti-Vibrio immune responses. In this study, a total of 12 TrIRF genes were identified in the genome of tiger puffer, distributed across 11 chromosomes. Phylogenetic analysis classified these TrIRF genes into four distinct subfamilies: IRF1, IRF3, IRF4, and IRF5. Domain prediction indicated that the IRF1 subfamily possesses only the IRF domain, whereas the other subfamilies additionally contain the IRF-3 domain. Expression profiling demonstrated distinct tissue-specific patterns of the 12 TrIRFs in healthy tiger puffer, with most genes exhibiting higher expression levels in immune-related tissues such as the head kidney, gill, intestine, and spleen, and further revealed their differential expression patterns during larval development. Furthermore, following Vibrio harveyi infection, significant differential expression of TrIRFs was observed in the intestine, spleen, and liver, with an overall trend of initial upregulation followed by subsequent downregulation over time. These findings provide significant reference data for investigating IRF functions in teleosts and contribute to the understanding of innate immunity in vertebrates. - Source: PubMed
Publication date: 2026/06/11
Li XinyangYang ZhenCao XinyuSong ZixuanYang ZheJiang ChenTian Yushun - Clinical therapies targeting mammalian target of rapamycin (mTOR) are associated with high rates of pneumonitis. Recent studies independently revealed the upregulation of the proinflammatory transcription factor interferon regulatory factor-1 (IRF-1) by mTOR inhibition (mTORi) of endothelial cells (EC) and further highlighted a mechanism converging on myosin light chain (MLC) phosphorylation-dependent cytoskeletal dynamics in promoting the endothelial hyperpermeability and pulmonary inflammation caused by mTORi. This study investigated a role for this mechanism in linking the regulation of IRF-1 expression with downstream responses in mTOR-inhibited EC. IRF-1 was transcriptionally upregulated in cultured EC by treatment with mTOR inhibitor rapamycin or torin 1, or by silencing either Raptor or Rictor expression to disrupt mTOR complex 1 (mTORC1) or 2 (mTORC2). Inhibition of MLC kinase (MLCK) activity or activation of MLC phosphatase (MLCP) to suppress MLC phosphorylation, or direct inhibition of actin polymerization, attenuated IRF-1 expression as well as transcription of an array of proinflammatory cytokines. Moreover, IRF-1 in turn upregulated MLCK expression to enhance MLC phosphorylation and promote endothelial hyperpermeability in mTOR-inhibited EC. Consistent with these observations in culture, targeted endothelial deficiency of IRF-1 in mice significantly reduced lung edema and inflammation elicited by separate or combined treatment of rapamycin and lipopolysaccharide. In conclusion, activation of actomyosin contractility by mTORi upregulated IRF-1, which promoted the development of lung injury by mediating inflammation and hyperpermeability responses in EC. - Source: PubMed
Zhou YingZhang ZhiyangHu ChengxiuZhu XiangjunFan XingZhang Dai-MinPasserini Anthony GSun ChongXiu