IRF1 (C_term)
- Known as:
- IRF1 (C_term)
- Catalog number:
- AP15609PU-N
- Product Quantity:
- 1.0 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)
- Respiratory syncytial virus (RSV) causes severe lower respiratory disease, yet how it reshapes airway epithelial cells and evades innate immunity remains incompletely understood. We infected adult primary human airway epithelial cultures with RSV and analyzed infected and bystander cells over time using single-cell RNA sequencing and imaging. RSV mainly infected ciliated cells, triggering a virus load-dependent shutdown of genes involved in ciliogenesis, antigen presentation, and innate sensing, including key interferon (IFN) and pattern recognition pathways. Only a subset of infected cells produced type I and III IFNs, while bystander cells exhibited strong IFN-stimulated gene (ISG) signatures. Neither IFN treatment nor ISG induction eliminated infection, but IRF1, an antiviral transcription factor not suppressed by RSV, remained robustly expressed. Ectopic IRF1 expression in vitro reduced viral replication. These findings reveal how RSV evades antiviral defenses and highlight IRF1 as a potential target for therapeutic intervention. - Source: PubMed
Publication date: 2026/06/19
Berg KevinHaid SibylleVafadarnejad EhsanCarpentier ArnaudGeffers RobertWiegmann BettinaSaliba Antoine-EmmanuelErhard FlorianPietschmann Thomas - The purpose is to define the contribution of the interferon regulatory factor-1-dual-specificity tyrosine phosphorylation-regulated kinase 1α (IRF-1-DYRK1α) axis to hepatocellular ferroptosis during liver ischemia/reperfusion injury (LIRI). - Source: PubMed
Publication date: 2026/06/16
Zhang JinpingZhang JinmingSong SiyuanLi MingyangSun LiyingZhu ZhijunLin Dongdong - [This retracts the article DOI: 10.2147/CMAR.S186236.]. - Source: PubMed
Publication date: 2026/06/05
- Hypertensive disorders of pregnancy (HDPs) affect 5%-10% of pregnant women and, in the absence of established therapies, remain a leading cause of maternal and perinatal mortality. HDPs have been associated with disruption of cytotrophoblast fusion into syncytiotrophoblasts, a process essential for placental development. Here, we identified altered expression of mitochondrial dihydroorotate dehydrogenase (DHODH) and interferon-induced transmembrane proteins (IFITMs), using HDP placentas, and investigated their functional roles in trophoblast fusion and membrane dynamics. In trophoblast cells, the inhibition of DHODH led to upregulated expression of IFITM1-3 through transcription factor IRF1 and suppression of syncytialization. IFITMs also increased the proportion of saturated fatty acids, thereby decreasing plasma membrane fluidity. Furthermore, IFITM2 increased the soluble fms-like tyrosine kinase-1/placental growth factor (sFlt1/PlGF) ratio, a key biomarker of HDP severity. These results suggest that DHODH deficiency activates IRF1-mediated IFITM2 expression, leading to impaired trophoblast fusion via biophysical remodeling of the membrane and contributing to HDP pathogenesis. - Source: PubMed
Publication date: 2026/06/08
Yoshida KanokoKusama KazuyaKojima JunyaKawaguchi YuSuzuki KaitoShimooki TomokaTsuru AtsuyaYoshie MikihiroOno MasanoriNishi HirotakaKato KiyokoTamura Kazuhiro - Ulcerative colitis (UC) is characterized by cytokine-driven inflammation and barrier disruption in the colon, making epithelial dysfunction central to disease pathology. Intestinal epithelial organoids (IEOs) preserve donor-specific genetics and architecture, offering a promising model, but their ability to replicate patient-specific epithelial inflammation remains undetermined. To directly compare in vivo epithelial transcriptional states with defined cytokine-induced responses in vitro, we analyzed patient-matched transcriptomics from laser microdissected inflamed and uninflamed colonic epithelium and IEOs derived from uninflamed biopsies of the same UC patients. IEOs were stimulated with UC-relevant cytokines (TNF, IFNγ, IFNλ1, or TNF + IFNγ) or a cytokine cocktail (TNF, IL17, IL1β, IL22, Poly(I:C), IFNγ). Key inflammatory genes were validated by immunoblotting and immunostaining. Cytokine-stimulated IEOs recapitulated key in vivo epithelial inflammation, including interferon signaling, antigen presentation, and unfolded protein response pathways. Among the tested conditions, TNF + IFNγ combination and the cytokine cocktail most closely replicated UC epithelial inflammation, with concordance for over 350 UC-relevant genes and protein-level validation of IRF1, ERAP2, NOS2, DUOX2 confirmed patient-dependent expression between inflamed epithelium and cytokine-stimulated IEOs. Our study shows that cytokine-stimulated IEOs provide a robust, personalized platform for modeling epithelial inflammation, enabling discovery of epithelial-specific disease mechanisms and therapeutic targets. - Source: PubMed
Publication date: 2026/06/14
Walaas Gunnar Andreas EnerhaugSridhar ArunKuraas Lusie FrostvollSæterstad SiriSchioldborg Amanda YinVan Beelen Granlund AtleSandvik Arne KristianØstvik Ann ElisabetBakke IngunnBruland Torunn