IRF1 ELISA kit
- Known as:
- IRF1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-IRF1-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- IRF1 ELISA kit
Related genes to: IRF1 ELISA kit
- 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
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- Interferon regulatory factor 1 (IRF1) has long been recognized as a tumor suppressor; however, recent studies have revealed context-specific and sometimes opposing roles in cancer progression. Here, we describe a T cell-specific mechanism underlying the antitumor activity of IRF1. Unlike germline -deficient mice, T cell-specific loss of IRF1 does not lead to a deficiency in cytotoxic CD8⁺ T cells. Nevertheless, tumor burden remains elevated in these mice, associated with reduced CD8⁺ T cell infiltration driven by impaired activation and proliferation in the absence of IRF1. Transcriptomic analysis of activated -deficient T cells identified NFATc1 as a key gene significantly downregulated upon IRF1 loss. Analysis of human melanoma datasets further corroborated this finding, highlighting a previously unappreciated role for IRF1 in regulating T cell activation and antitumor immunity. - Source: PubMed
Publication date: 2026/05/18
Shao LuluBannerjee HrideshUnal EcemMehta IshaDas JishnuBanday A RoufKane LarrySarkar Saumendra N - Type 1 diabetes (T1D) is characterized by the autoimmune destruction of pancreatic beta cells. While most beta cells are lost, a subset of beta cells persists years and even decades after disease onset. Studying these surviving cells is challenging, and thus how they escape immune killing remains poorly understood. Here, we applied a gene regulatory network inference-based clustering approach on existing islet scRNAseq data from cadaveric donors with T1D, autoantibody positive donors at risk for T1D, and non-diabetic donors to analyze beta cells from patients with established T1D. This approach identified a novel beta cell subtype enriched in T1D donors defined by the activity of several transcription factors which have well-characterized roles in beta cell survival, most notably IRF1. We found increased expression of immunomodulatory genes (e.g. ) as well as decreased expression of autoantigens and secretory genes, suggesting dedifferentiation. We identified inflammatory cytokines as a driver of this phenotype by reanalyzing public data from primary human beta cells stimulated with inflammatory cytokines in vitro. We additionally find a similar transcriptional program active in a subset of alpha cells, consistent with cell-extrinsic inflammatory cytokine signaling in vivo. Overall, we propose that this population represents a resilient beta cell phenotype, and that the transcriptional program active in these cells may identify targets for T1D prevention and reversal. - Source: PubMed
Publication date: 2026/05/27
Spurrell MaxwellTsang John SHerold Kevan C - Hepatic ischemia-reperfusion injury (IRI) is a complex event influenced by interconnected immune and metabolic processes. Steatotic livers are especially sensitive to IRI, but the crosstalk between innate inflammatory responses and lipid metabolic dysregulation in this context is not well understood. Using transcriptomic profiling in a murine high-fat diet (HFD) model, we assessed immune and metabolic responses to hepatic IRI and examined the effects of N-acetylcysteine (NAC). In steatotic livers, IRI induced the upregulation of inflammatory mediators, including TLR/NF-κB-associated genes (, , ) and neutrophil-associated genes (, ), accompanied by the downregulation of lipid and cholesterol metabolism-related genes, including , , , and . NAC supplementation attenuated inflammatory gene expression and restored key lipid biosynthetic regulators. We then performed targeted lipidomic analysis to determine whether NAC-mediated transcriptional changes were reflected at the lipid level and observed a significant increase in total phosphatidylcholine and sphingomyelin in steatotic livers following IRI. Finally, to assess the contribution of innate immune cells to hepatic IRI, we quantified neutrophils and macrophages in HFD+NAC IRI and HFD IRI livers. We found that NAC supplementation reduced hepatic neutrophil accumulation and markedly decreased LCN2 expression following IRI. - Source: PubMed
Publication date: 2026/05/19
Kang JimanPatil DigvijayHackett RyanCui YukiOza KeshaRutkowski AbigailLiggett Jedson RLi HenghongRanjit SumanKwon DongHyangKallakury BhaskarAlbanese ChrisGondolesi Gabriel EEkong UdemeCui WanxingKhan KhalidFishbein Thomas MKroemer Alexander - Colorectal cancer (CRC) poses major clinical challenges, and deeper molecular and immunological insights are essential for precision oncology. We integrated RNA sequencing (RNA-seq) and clinical data from a Korean CRC cohort to profile tumor biology and immune heterogeneity. Differential expression analysis revealed 1,652 upregulated and 1,372 downregulated genes in tumors, with enrichment of DNA damage response (DDR), WNT signaling, and extracellular matrix (ECM)- receptor pathways, whereas normal tissues were enriched for metabolic processes. Consensus Molecular Subtype (CMS) classification identified canonical subtype-specific features, with unclassified tumors resembling CMS2. Immune phenotyping stratified tumors into hot, intermediate, and cold groups, showing distinct associations with microsatellite instability (MSI) and CMS subtypes. Tumor Immune Dysfunction and Exclusion (TIDE) analysis predicted responders across all phenotypes, unexpectedly including intermediate and cold tumors. Notably, interferon-STAT3-PIM1 signaling characterized non-responders, implicating oncogenic drivers of immune resistance. Immunehot tumors displayed strong antigen presentation (HLA-C, B2M) and apoptosis (FAS) signatures, supporting sensitivity to PD-1 blockade with potential benefit from apoptosis-targeting agents. Intermediate tumors showed partial CD8＋ T cell activation, suggesting combinatorial strategies such as CTLA-4 blockade or oncolytic priming. Cold tumors with IRF1 expression exhibited latent immune potential, indicating opportunities for epigenetic modulation plus checkpoint inhibition. These findings highlight the immune transcriptomic diversity of CRC and demonstrate that immune phenotype-based stratification provides actionable insights beyond MSI or CMS classification. This framework may guide personalized immunotherapy strategies for Korean CRC patients and inform future integration with spatial transcriptomic profiling. - Source: PubMed
Publication date: 2026/06/02
Yoo JinseonKim JinyongChu Hoang Bao KhanhJoe SoobokHan Sae-WonCho SheehyunShim HyeranKang JisunLee Hong SeokKim DongWooKim JisuKim Jong-HwanJeon JongbumYang Jin OkKim Seon-YoungKim Young-JoonRyoo Seung-Bum - Keratinocytes are key barrier cells able to mount a robust interferon (IFN) antiviral response to defend against infection in the skin. Similar to humans, dogs spontaneously develop skin disorders associated with dysregulation of IFN immunity and can be used as a large animal model to investigate these diseases. One of the critical factors driving IFN regulation are interferon regulatory factors (IRFs). IRFs are crucial in upregulating the antiviral type I or type III IFNs, which then subsequently upregulate hundreds of antiviral effector proteins called interferon stimulated genes (ISGs). - Source: PubMed
Publication date: 2026/05/15
Quinlan SarahMay SusanWeeks RyanLuff Jennifer