IRF1 antibody (Cy3)
- Known as:
- IRF1 (anti-) (cynanin 3)
- Catalog number:
- orb114698
- Product Quantity:
- 100 ul
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- IRF1 antibody (Cy3)
Related genes to: IRF1 antibody (Cy3)
- 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 antibody (Cy3)
Related articles to: IRF1 antibody (Cy3)
- - Source: PubMed
Publication date: 2026/07/16
Wu YuanzhongZhou LiwenZou YeziZhang YijunZhang MeifangXu LipingZheng LisiHe WentingYu KuaiLi TingZhang XiaChen ZhenxuanZhang RuhuaZhou PenghuiZhang NuZheng LiminKang Tiebang - Innate immune cell death is a fundamental mechanism used by organisms to respond to perturbations, including infection, tissue damage, and cancer. However, excessive cell death can be inflammatory and cause pathology. PANoptosis has emerged as a distinct, lytic, inflammatory cell death pathway initiated by innate immune sensors and driven by caspases and receptor-interacting protein kinases through multiprotein PANoptosome complexes. Genetic, biochemical, and imaging evidence initially identified PANoptosis in macrophages but now indicates that it operates across diverse immune, non-immune, and cancer cell types, where it drives host defense, inflammation, and pathology. In this review, we critically evaluate current evidence for PANoptosis as a unique and central cell death pathway across cell types and disease contexts, elucidating the key molecular mechanisms that govern its activation. We discuss emerging insights into PANoptosome biology, the physiological and pathological functions of PANoptosis, and how cell type-specific regulation shapes disease outcomes. Finally, we highlight the therapeutic opportunities and challenges associated with the cell-selective modulation of PANoptosis to improve treatment of infectious, inflammatory, and malignant diseases. - Source: PubMed
Zengeler Kristine ETweedell Rebecca EKanneganti Thirumala-Devi - While interferon regulatory factor 1 (IRF1) has been implicated in reactive oxygen species (ROS)-dependent neutrophil extracellular trap (NET) release during acute lung injury, its regulatory role in mitochondrial dysfunction-driven NETosis specific to pediatric pneumonia remains unexplored. Neutrophils were isolated from the bronchoalveolar lavage fluid (BALF) of pediatric pneumonia patients and the bone marrow of mice. IRF1 expression was quantified via qRT-PCR and Western blotting. Mitochondrial ROS (mtROS) and total ROS were measured by flow cytometry. Mitochondrial dysfunction was assessed by ATP quantification. NETosis was evaluated through immunofluorescence staining and ELISA quantification of neutrophil elastase (NE), myeloperoxidase-DNA (MPO-DNA), and citrullinated histone H3 (Cit-H3) levels. For in vivo studies, pneumonia-related lung injury was induced by intratracheal LPS instillation in mice, with pathological severity graded by H&E staining, pulmonary edema quantified via the wet/dry weight ratio, and inflammation assessed by the BALF protein concentration. Mechanistically, the IRF1/MMP9 interaction was predicted by bioinformatics (STRING database) and validated by co-immunoprecipitation (Co-IP) and immunofluorescence staining, while MMP9 overexpression was achieved via lentivirus transduction to delineate pathway regulation. IRF1 was significantly upregulated in BALF neutrophils from patients and correlated with elevated ROS production and mitochondrial dysfunction, as well as NETs release. IRF1 knockdown attenuated ROS-driven NETosis in vitro. Matrix metalloproteinase 9 (MMP9) was predicted to interact with IRF1, and MMP9 overexpression effectively reversed the beneficial effects of IRF1 deficiency on ROS release, mitochondrial dysfunction, neutrophil apoptosis, and NETosis. Consistently, in mouse models, MMP9 overexpression abolished the protective effects of IRF1 deficiency, exacerbating acute lung injury and restoring NETs levels in BALF. - Source: PubMed
Publication date: 2026/07/16
Wei YandanFu WeiLiu YanxiaZhen RuyiDeng HuabinHuang ShufenLi ShuangPeng Dongzheng - Chronic kidney disease (CKD) is imperceptible and with a complex pathogenesis involving oxidative stress and inflammatory responses. The phosphatidylinositol 3 kinases/protein kinase B (PI3K/AKT) signaling pathway plays a crucial role in this process. Previous studies indicated that chemokine ligand 25 (CCL25) and its receptor CCR9 participate in regulating the PI3K/AKT pathway. However, it remains unclear whether CCL25/CCR9 influences CKD by modulating oxidative stress and inflammation via the PI3K/AKT pathway. We aimed to clarify the roles of CCL25/CCR9 in CKD progression through PI3K/AKT activation and its upstream regulatory factors. In this study, an adenine-induced CKD rat model and an indoxyl sulfate-induced CKD cell model were constructed. Bioinformatics method based on two online websites (JASPAR and Cistrome DB) was conducted to predict the upstream of CCL25/CCR9. Anti-CCL25 and PI3K/AKT activator 740Y-P were added, and sh-IRF1 was transfected into the HK-2 cells for the mechanism exploration. Renal function markers (blood urea nitrogen, creatinine, urine protein/creatinine ratio), renal pathology, oxidative stress markers (reactive oxygen species, malondialdehyde, superoxide dismutase), inflammatory cytokines (Interleukin (IL)-1β, IL-6, Tumor Necrosis Factor (TNF)-α), and the expression of CCL25, CCR9, PI3K/AKT pathway-related proteins, and the transcription factor interferon regulatory factor 1 (IRF1) were measured. Chromatin immunoprecipitation PCR (ChIP-PCR) was used to confirm IRF1 binding to the CCL25 promoter. The results indicated that CCL25 and CCR9 were upregulated in CKD rat and cell model. Enhanced oxidative stress and inflammatory response, followed by renal fibrosis and renal dysfunction, were observed in CKD rats. Anti-CCL25 addition decreased the PI3K/AKT markers, oxidative stress markers, and inflammatory responses, whereas 740Y-P addition reversed the above alteration. IRF1 was confirmed to be an important transcription factor for CCL25 in bioinformatics analysis. IRF1 was increased in CKD models and binding with CCL25 in ChIP-PCR detection. sh-IRF1 transfection decreased the CCL25 and CCR9 expression. In conclusion, IRF1-regulated CCL25/CCR9 was demonstrated to promote CKD progression through PI3K/AKT-mediated oxidative stress and inflammatory response. - Source: PubMed
Publication date: 2026/01/14
Yan ShaorongChen YuepingChen Hong LiangJin ChenfeiLin SenChen Lei - Aminoglycosides remain clinically important antibiotics, but their use is limited by nephrotoxicity. Although proximal tubular accumulation mediated by megalin is well established, the downstream cellular response is still incompletely understood. Here, we compared repeated-dose transcriptomic responses to gentamicin and tobramycin in a panel of human proximal tubular models comprising primary proximal tubular epithelial cells (PTEC; three donors), human iPSC-derived proximal tubular-like cells (PTL; three donors), RPTEC/TERT1 cells, and HK-2 cells. Cells were exposed daily for seven days to 12, 250, or 450 µg/mL gentamicin or tobramycin, and gene expression was assessed using the TempO-Seq EU-ToxRisk v2.1 panel followed by DESeq2 analysis. Primary PTEC and PTL showed the clearest and most coherent response, characterised by strong induction of interferon-stimulated genes including IFI27, IFI6, IFIT1-3, ISG15, MX1, OAS1, UBE2L6, USP18, IFI44L, HERC6, and RSAD2. Targeted regulator analysis showed strong enrichment of overlapping ISGF3, IRF7, and IRF1 target networks, consistent with a dominant interferon-stimulated gene program, together with a smaller NF-κB-associated inflammatory branch. In contrast, RPTEC/TERT1 and HK-2 cells showed weaker and less coherent responses. Tobramycin generally induced a stronger and more consistent transcriptional response than gentamicin across responsive models. These data identify a robust innate immune-like transcriptional signature in human proximal tubular models following repeated aminoglycoside exposure and support primary PTEC and PTL as more informative in vitro systems for mechanistic investigation of aminoglycoside nephrotoxicity. - Source: PubMed
Publication date: 2026/07/14
Chandrasekaran VidyaMeijer TamaraLeonard Martin OWilmes AnjaJennings Paul