Anti-Mouse IRF1 Purified 100 ug
- Known as:
- Antibody toMouse IRF1 Purified 100 ug
- Catalog number:
- 14-5836-82
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse IRF1 Purified 100
Related genes to: Anti-Mouse IRF1 Purified 100 ug
- 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: Anti-Mouse IRF1 Purified 100 ug
Related articles to: Anti-Mouse IRF1 Purified 100 ug
- genetic variants associated with kidney disease become pathogenic when gene expression is induced to high levels, however, the mechanism of gene regulation is not well characterized. Using human podocyte cell lines, the induction of gene expression from various pathogen recognition receptors was universally blocked with a soluble receptor for type I interferons, indicating induction from these different innate immune mechanisms was secondary to autocrine production of type I interferon. ATAC-seq and chromatin immunoprecipitations identified the gene is regulated by an ISRE-containing promoter and an intronic enhancer containing an interferon-γ activation sequence (GAS) element which explains its responsiveness to both type I and type II interferons. RNAi-mediated gene silencing identified the transcription factor required for basal expression levels (IRF1) was not required for interferon-induced expression, which utilized additional transcription factors known to mediate interferon receptor signaling (IRF9 and STATs). An inhibitor of Janus Kinases (JAK), which activate signaling from interferon receptors, was able to attenuate the interferon-induced, but not basal levels of expression. These differential gene regulatory mechanism may be useful in optimizing treatment strategies for APOL1 mediated kidney disease. - Source: PubMed
Publication date: 2026/09/14
Huang ChunfaWu ZhenzhenBartolomeo Korey RO'Toole John FSedor John RBruggeman Leslie A - Vibrio harveyi is a major bacterial pathogen in marine aquaculture, posing a serious threat to fish health. IRF1 is a conserved regulator of teleost immunity; however, the transcriptional regulatory networks associated with IRF1 during bacterial infection remain incompletely understood. To characterize CaIRF1-associated transcriptional responses during Vibrio harveyi infection, Chromileptes altivelis were injected with PBS (Control group, ControlVa), pCaIRF1 (CaIRF1 overexpression group, VpCaIRF1), or siCaIRF1 (CaIRF1 knockdown group, VsiCaIRF1), and then infected with V. harveyi. Transcriptome analysis was performed in VpCaIRF1 vs. ControlVa and VsiCaIRF1 vs. ControlVa. In VpCaIRF1 vs. ControlVa and VsiCaIRF1 vs. ControlVa, 2,495 and 3,650 differentially expressed genes (DEGs) were identified; furthermore, 1498 DEGs were shared, enriched in immune-related pathways, such as Toll-like receptors (TLRs), interferons (IFNs), cytokines, and tumor necrosis factor (TNF) signaling. Gene Ontology (GO) enrichment analysis indicated that these DEGs were mainly involved in immune responses, antigen processing and presentation, and oxidative stress regulation. KEGG pathway analysis showed that CaIRF1 overexpression was associated with enrichment of cytokine-mediated signaling, apoptosis, and metabolic pathways, whereas CaIRF1 knockdown was associated with enrichment of pathogen-recognition pathways, including TLR, NOD-like receptor, RIG-I-like receptor, and cytosolic DNA-sensing pathways. Additionally, CaIRF1-associated candidate genes were identified, among which multiple immune-related genes, including TLR1, Cyclic GMP-AMP Synthase (CGAS), Class II Major Histocompatibility Complex Transactivator (CIITA), and Tumor Necrosis Factor Receptor Superfamily Member 11b (TNFRSF11b) etc., were involved in pathogen recognition, inflammatory signaling, antigen presentation, and immune cell regulation. Quantitative real-time PCR analysis confirmed the reliability of the transcriptome data, showing consistent expression patterns of key immune-related genes. Collectively, CaIRF1 modulation was associated with broad transcriptional changes in immune-related processes during V. harveyi infection, including pathogen recognition, cytokine signaling, apoptosis, and oxidative stress responses. This study provides a transcriptomic characterization of CaIRF1-associated immune responses and identifies candidate pathways for subsequent functional validation in teleost fish. - Source: PubMed
Publication date: 2026/09/11
Wang GuotaoChen GuisenWu TingFu ZhiqingCao ZhenjieZhang ChenWang ShifengAo JingqunZhou YongcanWu YingSun Yun - Pancreatic adenocarcinoma (PAAD) is an immunosuppressive malignancy refractory to radiotherapy and immunotherapy. Conventional tumor vaccines fail in PAAD due to a suppressive tumor microenvironment (TME), inadequate antigen presentation, and impaired immunogenic cell death (ICD). Using a machine learning-driven transcriptomic analysis, we identified FSTL3 as a vital TME regulatory factor enriched in desmoplastic pancreatic lesions and constructed a cRGD-modified liposomal carrier co-encapsulating gemcitabine and siFSTL3 (siFSTL3/Lip-cRGD). Unlike antigen-preloaded conventional nanovaccines, this liposome acts as an irradiation-activated inducer of in situ tumor vaccination. This engineered multifunctional nanovaccine enhanced radiochemosensitivity and, combined with ionizing radiation (IR), promoted dendritic cell maturation, ICD, and ferroptosis. Mechanistically, this composite nanovaccine synergized with IR to trigger ferroptosis and ICD via the STAT1-IRF1-ACSL4 axis, thereby remodeling the TME and overcoming the limitations of conventional vaccines by enhancing antigen release. In vivo, triple therapy with the liposomal carrier, IR, and anti-PD-L1 achieves robust anti-tumor activity with negligible systemic toxicity and overcomes immune checkpoint blockade resistance. This study develops a translatable radiotherapy-initiated in situ nanovaccination strategy relying on synergistic ferroptosis and ICD to treat refractory PAAD. - Source: PubMed
Publication date: 2026/09/10
Huang ChengyiHan YushuLiu XiangWang ChuanhaoZhu XiaofeiChen DiGong YangyangChen LiangChen WenjuanMiao ZhenyuanTang BufuZhang Huojun - Swine Acute Diarrhea Syndrome Coronavirus (SADS-CoV) is an emerging porcine enteric coronavirus that causes severe diarrhea in piglets. Type III interferon (IFN) are crucial for intestinal antiviral defense, and the capacity of SADS-CoV to disrupt IFN-III responses is critical for its replication. This study found that SADS-CoV inhibits IFN-III production through its nonstructural protein 1 (Nsp1), which degrades interferon regulatory factor 1 (IRF1) by promoting its ubiquitination and proteasomal degradation. Mass spectrometry and co-immunoprecipitation analyses revealed that SADS-CoV Nsp1 interacts with proteasomal subunits. Further research indicates that PSMB4, PSMB5, and PSMC5 are key proteasomal subunits involved in SADS-CoV Nsp1-induced IRF1 degradation. Similarly, Porcine Epidemic Diarrhea Virus (PEDV) and Transmissible Gastroenteritis Virus (TGEV) Nsp1 exhibit similar functions, highlighting the conserved role of coronavirus Nsp1 in immune evasion. Collectively, our findings uncover a new mechanism where SADS-CoV Nsp1 exploits the proteasome to degrade IRF1, countering IFN-III responses. - Source: PubMed
Publication date: 2026/09/06
Xiang YingjieZhu QinyuanCheng YueZhao XingShi KaichuangFeng ShupingHuang YuChen ZhenhaiLin ChanghuaMou Chunxiao - Hope has been associated with improved quality of life and lower mortality in cancer, but the underlying biological mechanisms are poorly characterized. We previously reported that hope was associated with less inflammation and more normalized diurnal cortisol pre-treatment among women with ovarian cancer. We also reported associations of socio-environmental factors with pro-metastatic processes. Here, we used genome-wide transcriptional profiling to quantify associations between hope and tumor molecular signatures reflecting invasiveness, inflammation, and cellular immunity. - Source: PubMed
Publication date: 2026/09/08
Lutgendorf Susan KCorn Benjamin WThaker Premal HGoodheart Michael JPenedo Frank JSood Anil KCole Steven W