IRF1 Pre-design Chimera RNAi
- Known as:
- IRF1 Pre-design Chimera RNAi
- Catalog number:
- H00003659-R01
- Product Quantity:
- 20 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- IRF1 Pre-design Chimera RNAi
Related genes to: IRF1 Pre-design Chimera RNAi
- 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 Pre-design Chimera RNAi
Related articles to: IRF1 Pre-design Chimera RNAi
- PANoptosis, a form of programmed cell death involving crosstalk among pyroptosis, apoptosis, and necroptosis, has recently emerged as a key player in tumor progression and therapy resistance. Despite growing evidence linking PANoptosis to various cancers, the prognostic significance of PANoptosis-related genes (PANRGs) and their roles in breast cancer is not well defined. Investigating their relevance could reveal novel biomarkers for patient stratification and identify new therapeutic targets to overcome resistance to existing treatments. - Source: PubMed
Publication date: 2026/06/15
Hong JinghuiWei ZhihaoLi MengxinGao XiaochuanWu YuhengWang XuyutianWang XinZhang TianxingSong Dong - As one of the critically important transcription factors, interferon regulatory factors (IRFs) modulate the host transcriptional program triggered by pathogen-associated molecular patterns in variety of marine invertebrates. Their activation is indispensable for initiating and modulating innate immune defenses across animal taxa. However, the functional characteristics and regulatory mechanisms of IRFs in echinoderms remain poorly understood. In this study, a newly identified IRF family member, Si-IRF1/2, was cloned and characterized in the sea urchin Strongylocentrotus intermedius. Si-IRF1/2 comprises a full-length ORF of 1668 bp, corresponding to a 555-amino-acid protein. Computational analysis identified a conserved IRF domain at the N-terminal region. This conserved signature was identified through integrated domain prediction and corroborated by multiple sequence alignment with orthologs from diverse species. Phylogenetic analysis showed that Si-IRF1/2 clusters closely with members of the vertebrate IRF1/2 proteins and molluscan IRF1/2 homologs. The tissue-specific expression profile of Si-IRF1/2 was assessed by qRT-PCR. Although transcripts were ubiquitously present, expression was markedly enriched in coelomocytes, indicating a specialized role in this immunologically relevant tissue. Moreover, expression of Si-IRF1/2 was upregulated when stimulated with lipopolysaccharide (LPS) and poly (I:C). Subcellular localization assays showed that Si-IRF1/2 is predominantly localized in the nucleus. The results of the RNAi experiment indicate that after Si-IRF1/2 was knocked down, the mRNA expressions of Si-strongylocins and Si-IL17s in coelomocytes changed significantly at 12 h after LPS stimulation. The transcriptional regulatory capacity of Si-IRF1/2 was further confirmed by dual-luciferase reporter assays, which demonstrated its ability to enhance the activity of promoters from multiple immune-related genes, including interleukin-6 (IL-6), Interferon-α/β (IFNα/β), Signal transducer and activator of transcription 3 (STAT3), activator protein-1 (AP-1), interferon-stimulated response element (ISRE), nuclear factor-κB (NF-κB), and tumor necrosis factor α (TNFα). Under LPS stimulation, overexpression of Si-IRF1/2 promoted activation of mitogen-activated protein kinase pathways, specifically c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase 1/2 (ERK1/2). Taken together, these findings provide new insights into the immune-regulatory role of Si-IRF1/2 to establish a conceptual framework for breeding sea urchin lines with improved resistance to disease, while simultaneously providing new knowledge of innate immune mechanisms mediated by IRFs in invertebrates. - Source: PubMed
Publication date: 2026/06/29
Liu FengchenXu DongDing XuanRen GuoshunThiyagarajan VengatesenChu XiaolongLiu TongHuang BaoyuWang Xiaotong - The immunosuppressive tumor microenvironment (TME) remains a major barrier to the efficacy of immune checkpoint blockade (ICB) therapy, underscoring the need for strategies that can safely reprogram the TME to enhance cancer immunity. - Source: PubMed
Publication date: 2026/05/29
Nguyen Dinh-HuyYou Sung-HwanVan Nguyen KhuynhNguyen Phuong Thi-MinhNgo Hien Thi-ThuTran Khang VuongTran Thanh QuangSong MiryoungHong YeongjinMin Jung-Joon - Hypoxia within the tumor microenvironment (TME) triggers the exosomal transfer of microRNAs (hypoxamirs) that reprogram tumor-associated macrophages (TAMs) toward a pro-tumorigenic M2 phenotype. This systematic review defines the molecular pathways and clinical consequences of the hypoxamir-TAM axis across solid malignancies to guide therapeutic translation. A systematic search of PubMed, Embase, and Cochrane library was conducted through February 1, 2026. Following PRISMA 2020 guidelines, 17 studies were included for analysis. Methodological quality was evaluated using the standard Office of Health Assessment and Translation (OHAT) tool. Analysis identified two primary regulatory tracks: a signaling axis mediated by targets such as PTEN, IRF1, and PHLPP2, and a metabolic axis driven by miR-210, let-7a, and miR-30c targeting the iron-sulfur cluster assembly protein (ISCU). These coordinated pathways drive an "angiogenic switch," facilitate "metabolic migration," and induce significant resistance to chemotherapies, including gemcitabine and temozolomide. Fourteen studies achieved a high-confidence Tier 1 OHAT rating. The hypoxamir-TAM axis is a fundamental driver of immune evasion and therapeutic failure. Targeting this dual-axis framework offers a viable strategy for restoring anti-tumor immunity, while circulating hypoxamirs represent high-value liquid biopsy biomarkers for real-time TME monitoring. - Source: PubMed
Publication date: 2026/05/28
Altobi AlmunthirHeo DanhuiBarman LinaRuiz Santiago - Peripheral nerve injury induces neuroinflammation in the dorsal root ganglion (DRG), which is a major cause of neuropathic pain. Interferon regulatory factors (IRFs) are a family of transcription factors that regulate the expression of inflammatory genes. Although several IRFs affect nociceptive transmission in the spinal cord, their roles in the DRG remain largely unknown. - Source: PubMed
Watanabe YujiMaruyama MotoyoYokoyama MikiArakawa RyosukeSakai Atsushi