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
- Despite the promise of immune checkpoint inhibitors (ICIs) for gastric cancer (GC) treatment, limited cytotoxic T cell infiltration remains a major barrier to therapeutic efficacy. This study investigates whether targeting HEAT repeat containing 1 (HEATR1) can induce immunogenic PANoptosis to enhance anti-tumor immunity. - Source: PubMed
Publication date: 2026/09/04
Huang YaXu QingchengZhu MeijuanShen YaweiZhang Xianwen - Although PANoptosis plays a pivotal role in the pathogenesis of acute kidney injury (AKI), the underlying regulatory mechanisms and effective therapeutic strategies remain largely unexplored. In this study, we report a novel function of inactive rhomboid 2 (iRhom2), encoded by the Rhbdf2 gene, in promoting PANoptosis in tubular epithelial cells (TECs). First, iRhom2 expression was induced in the kidneys of mice with ischemia/reperfusion injury (IRI) or cisplatin-induced AKI, which was further confirmed in the kidneys of patients with biopsy-proven acute tubular necrosis (ATN). Moreover, iRhom2 levels positively correlated with serum creatinine (SCr) and blood urea nitrogen (BUN) levels in ATN patients. Functionally, the tubule-specific deletion of Rhbdf2 alleviated AKI progression. Mechanistically, iRhom2 facilitated the trafficking of ATF6 from the endoplasmic reticulum (ER) to the Golgi apparatus, leading to its proteolytic cleavage. Then, cleaved ATF6 (cATF6) subsequently translocated to the nucleus and upregulated the expression of HSP90, which acts as a positive regulator of IFN regulatory factor 1 (IRF-1), thereby promoting the formation of the RIPK1 PANoptosome in TECs. Importantly, both the silencing of Rhbdf2 using neutrophil membrane-enveloped nanoparticles and the pharmacological inhibition of iRhom2 with sulforaphane alleviated renal damage in AKI model mice. Collectively, these results reveal iRhom2 as a key regulator of PANoptosis and suggest that targeting iRhom2 may represent a potential therapeutic strategy for AKI. - Source: PubMed
Publication date: 2026/09/29
Lu Hong-ShenHan Qing-ShengRen Dan-DanLiu Ying-YingYu ShunZheng Ming-BoWu Ji-ChaoWang Xiao-JieLi Rong-KunJi RanLiu Zhi-YongWang Zi-YingSun YuLiu MinZhou MengLin Gui-MeiTang WeiZhang YanYi Fan - Hypertension is a major risk factor for intracranial atherosclerotic stenosis (ICAS), a leading cause of ischemic stroke in Asian populations. However, conventional risk factors only partially account for the pathogenesis of ICAS, underscoring the potential roles of epigenetic mechanisms. - Source: PubMed
Publication date: 2026/09/23
Zhu MinZhang JinMa JingWang QinWang YanZhu Dingliang - Interferon regulatory factor 2 (IRF2) is a transcription factor that prevents skin inflammation in mice and humans but, paradoxically, promotes pyroptosis by upregulating gasdermin D. How IRF2 activates some proinflammatory genes but suppresses inflammation is unclear. We show that skin inflammation in Irf2-deficient mice is driven by IRF1 activation of interferon-stimulated genes (ISGs). Chromatin profiling reveals that IRF1 and IRF2 occupy the same ISG regulatory sites, but as a weaker transcriptional activator, IRF2 limits ISG transcription by IRF1. Toll-like receptor (TLR) signaling favors IRF1-driven transcription by inducing Irf1. In addition, IRF1 recruits the ubiquitin ligase SPOP to ISG sites, resulting in proteasomal degradation of IRF2. This shift from IRF2 to IRF1 occupancy enhances ISG transcription. Collectively, these findings define a hierarchical transcriptional circuit in which IRF2 limits IRF1 activity under homeostatic conditions but is displaced during an immune response, allowing IRF1-dependent gene programs central to innate immunity and autoinflammation. - Source: PubMed
Publication date: 2026/09/22
Cadena CristhianReja RohitBolech EmmaWebster Joshua DKameswaran Vasumathide Simone MarcoChen CynthiaJiang JianHotzel KathyBjornson ChristopherAlegre KamelaTan ZhenyuElsaesser Heidi JNewland RaymondKelly RyanDarmanis SpyrosDaniel BenceBrooks David GDeshpande IshanNewton KimKayagaki NobuhikoDixit Vishva M - All-trans retinoic acid (ATRA) is a potent differentiation inducer successfully used to treat acute promyelocytic leukemia (APL), with its therapeutic efficacy traditionally attributed to targeting the PML/RARĪ± fusion oncoprotein. ATRA also exhibits anti-tumor activity in multiple non-APL malignancies. However, PML/RARĪ± targeting alone does not fully explain the diverse ATRA-induced anti-tumor responses, and the early transcriptional regulators coordinating these responses remain incompletely understood. Here, we performed a time-series transcriptomic analysis in an ATRA-sensitive APL cell line and identified interferon regulatory factor 1 (IRF1) as a pivotal early regulator of ATRA response that orchestrates multiple downstream transcriptional programs. Mechanistically, chromatin immunoprecipitation sequencing (ChIP-seq) revealed that ATRA enhanced IRF1 chromatin occupancy and transcriptional activity, thereby activating gene networks linked to ATRA-induced myeloid differentiation, proliferation control, cell-cycle regulation, and the reformation of promyelocytic leukemia (PML) nuclear bodies. Further IRF1 knockdown markedly impaired these phenotypic effects, confirming its essential role in coordinating ATRA-induced cell fate transitions. Moreover, cross-cancer studies demonstrated that IRF1 activation and the associated IRF1-dependent transcriptional signatures were selectively enriched in ATRA-sensitive tumors but not in ATRA-resistant contexts. Leveraging this shared regulatory mechanism, we developed an IRF1_ATRA score that could predict tumor responsiveness to ATRA across hematopoietic and solid malignancies, thereby supporting the expansion of ATRA-based therapy to a broader range of cancers. Collectively, our findings indicate that IRF1-dependent chromatin and transcriptional regulation contribute to the diverse anti-tumor effects of ATRA and provide a framework for biomarker-guided evaluation of ATRA in cancer therapies. - Source: PubMed
Publication date: 2026/09/19
Jin WenJin PengTan YunLou JiachengLi FuyuTao JingfenWang DanZhang YiYu YanerDong FangyiChen LiFang HaiWang Kankan