IRF1 EMSA Kit
- Known as:
- IRF1 EMSA Kit
- Catalog number:
- AY1021
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- IRF1 EMSA Kit
Related genes to: IRF1 EMSA 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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- 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/RARα fusion oncoprotein. ATRA also exhibits anti-tumor activity in multiple non-APL malignancies. However, PML/RARα 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 - Increased bone marrow adiposity is a characteristic of osteoporosis and negatively regulates osteogenesis. Bone marrow mesenchymal stem cells (BMSCs) give rise to bone marrow adipocytes. The transcription factor interferon regulatory factor 1 (IRF1) modulates multiple biological processes, including the adipogenesis of several cell types. However, the role of IRF1 in the commitment of BMSCs to the adipogenic lineage and whether it regulates bone marrow adipogenesis has not been investigated thoroughly. Murine BMSCs (mBMSCs) with Irf1-overexpression or knockdown were established via lentiviral transfection. IRF1's effects on adipogenic differentiation and autophagy of mBMSCs were studied in vitro; its role in adipogenesis in vivo was evaluated via nude mouse subcutaneous transplantation. Irf1-overexpressing mBMSCs were intravenously injected into OVX and aged osteoporotic mice. Besides, RNA sequencing and experimental verification explored the mechanism. IRF1 inhibited the adipogenic differentiation of mBMSCs both in vitro and in vivo. Besides, IRF1 positively regulated autophagy in mBMSCs in vitro. In osteoporotic mice, injection of Irf1-overexpressing mBMSCs effectively decreased bone marrow adiposity. IRF1 may downregulate adipogenic differentiation of mBMSCs by regulating the 5'-adenosine monophosphate (AMP)-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR) signaling axis. This study reveals that IRF1 induces protective autophagy and inhibits adipogenic differentiation of mBMSCs. Irf1-overexpressing mBMSCs alleviate osteoporosis-related bone marrow adiposity. Besides, IRF1 possibly regulates the AMPK-mTOR signaling axis. Our findings establish IRF1 as a key factor inhibiting adipogenesis, providing a new potential therapeutic target for preventing and treating osteoporosis-related bone marrow adiposity and other diseases with abnormal adipose metabolism. - Source: PubMed
Hu MenglongWei ErfanWu LikunPan XingtongZhu QiyueXu XiuyunDong XinyiLiu HaoLiu Yunsong - JMJD6, a jumonji C domain-containing protein located in the cancer-amplified region 17q25, has emerged as a putative oncogene in several malignancies. Only a few reports identified its function in gastric cancer (GC). In this study, we investigated the oncogenic and immunosuppressive roles of JMJD6 and its clinical relevance in GC. We analyzed 6 GC cell lines and 174 primary tumors. Overexpression of JMJD6 was frequently detected in GC cell lines (4/6 cell lines, 66.7%) and 69 primary GC specimens. Overexpression of JMJD6 was significantly associated with advanced tumor stage and was an independent poor prognostic factor (p<0.001, hazard ratio 4.15). Knockdown of JMJD6 suppressed GC cell proliferation, migration and invasion in a TP53 mutation-independent manner, and reduced programmed death-ligand 1 (PD-L1) expression via bromodomain-containing protein 4 (BRD4) and interferon regulatory factor 1 (IRF1) down-regulation. Ectopic overexpression of JMJD6 induced PD-L1 expression via BRD4 and IRF1 upregulation in low-PD-L1-expressing cells. In co-culture assays with activated T cells, JMJD6 knockdown enhanced tumor immunogenicity and T cell-mediated cytotoxicity. In primary GC samples, JMJD6 expression correlated positively with PD-L1 expression. These findings suggest that JMJD6 functions as a dual regulator of tumor aggressiveness and immune escape, highlighting its utility as a prognostic factor and a promising therapeutic target in GC. - Source: PubMed
Ishida RyoKomatsu ShuheiArakawa HiroshiOhashi TakumaImamura TaisukeKiuchi JunNishibeppu KeijiTakashima YusukeKamiya HajimeHamada SatoshiYamauchi MasateruShimizu HirokiArita TomohiroKosuga ToshiyukiKonishi HirotakaFujiwara HitoshiIehara TomokoTsuda HitoshiShiozaki Atsushi - Mitochondria can drive the development of inflammatory pathogenesis through releasing pro-inflammatory DAMPs, a process often triggered during virus infection. Whether a common mechanism exists that promotes virus-triggered mitochondria-derived inflammation is currently unknown. Here, we report that BAK is an interferon-stimulated gene that is up-regulated by the STAT1-IRF1 axis during virus infection to induce mitochondria-derived inflammatory pathogenesis. Viral infection triggers STAT1-dependent up-regulation of IRF1, which binds to an identified ISRE site in the BAK-promoter, inducing BAK up-regulation. Up-regulated BAK accumulates in the mitochondria triggering mitochondrial outer-membrane permeabilization and inflammatory responses. Both RNA and DNA viruses trigger the IRF1-mediated BAK up-regulation and mitochondria-derived inflammation. Using the Bak mouse model, we showed that both IAV and SFTSV, two viruses that induce severe inflammation in patients, trigger BAK up-regulation and BAK-dependent lethal inflammation. These results reveal a common mechanism that drives mitochondria-derived pathogenic inflammation, which can be targeted for developing anti-inflammatory therapeutics. - Source: PubMed
Publication date: 2026/09/16
Ye MeidiWang YifeiGuan ZhenqiongZhou ZhenxingGuan ZihanZhang YulanLi ShufenPeng Ke - Insomnia is a prevalent sleep disorder that strongly affects one's quality of life and physical well-being. Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the intestines, and a majority of IBD patients suffer from comorbid insomnia. However, the shared molecular features linking insomnia and IBD remain poorly characterized. - Source: PubMed
Publication date: 2026/09/01
Guo HanXu XudongShi HuanyingCui MengZhang MinWang HongdanZhang YunxuanZhou HaifengSun XuLiu Xiaoyan