Mouse polyclonal to IRF1, Host Mouse
- Known as:
- Mouse pab IRF1, Host Mouse
- Catalog number:
- YF-PA12765
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal IRF1 Host
Related genes to: Mouse polyclonal to IRF1, Host Mouse
- 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: Mouse polyclonal to IRF1, Host Mouse
Related articles to: Mouse polyclonal to IRF1, Host Mouse
- Aspergillus fumigatus poses a critical threat to immunocompromised hosts through invasive aspergillosis, with mortality rates reaching 50-90%. Although macrophages initiate early antifungal defenses via pattern recognition receptors, the temporal dynamics of immune reprogramming remain incompletely characterized. This study integrated time-series transcriptomics (GSE202286) of human monocyte-derived macrophages exposed to A. fumigatus conidia (0-8 h) with experimental validation to delineate immune-phase transitions and identify candidate regulatory modules. Bioinformatics analysis revealed a progressive increase in differential gene expression, peaking at 8 h (2,636 upregulated and 1,940 downregulated genes). Gene set enrichment analysis (GSEA) showed early enrichment of TNF-α/NF-κB signaling (NES = 2.37, 2 h), followed by a prominent interferon-γ response at 8 h (NES = 2.37) that coincided with ongoing inflammatory pathway activity. Temporal clustering identified 448 dynamically regulated genes associated with oxidative stress response (GO:0006979) and exploratory C-type lectin receptor-related pathway patterns (KEGG hsa04625). Protein interaction and transcription factor analyses predicted STAT2 as a candidate upstream regulator associated with IRF1 and ISG15. qRT-PCR validation in THP-1-derived macrophages showed sequential mRNA induction, with STAT2 peaking at 2 h, IRF1 at 4 h, and ISG15 remaining elevated through 8 h. A representative Western blot further supported this temporal pattern, showing early STAT2 phosphorylation, subsequent IRF1 protein induction, and later accumulation of free ISG15. Together, these findings suggest a STAT2-IRF1-ISG15-associated transcriptional program that may contribute to the transition from an inflammatory to an interferon-augmented macrophage response during A. fumigatus challenge. - Source: PubMed
Publication date: 2026/06/20
Zhou QuanLi RendongSong DandanXu XingpingTong Jianbo - 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