IRF5 Mouse Monoclonal Antibody
- Known as:
- IRF5 Mouse Monoclonal Antibody
- Catalog number:
- BIN-003663-M05
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- IRF5 Mouse Monoclonal Antibody
Related genes to: IRF5 Mouse Monoclonal Antibody
- Gene:
- IRF5 NIH gene
- Name:
- interferon regulatory factor 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-05-31
- Date modifiied:
- 2016-10-05
Related products to: IRF5 Mouse Monoclonal Antibody
Related articles to: IRF5 Mouse Monoclonal Antibody
- SLC15A4 is a member of the solute carrier superfamily that has been strongly linked to the pathogenesis of the auto-immune disease SLE. The endo-lysosomally localized SLC15A4 has traditionally been considered a proton-dependent histidine and peptide transporter, but has also been shown to facilitate TLR7, 8, and 9 induced IFN-alpha signaling in B cells and pDCs. New research has shown that SLC15A4 facilitates endo-lysosomal TLR signaling through a scaffolding interaction with a newly identified signal transducer, termed TASL. This interaction enables TLR7, 8, and 9 induced IRF5 activation, which is a crucial pathway in the pathogenesis of lupus. SLC15A4 is therefore an attractive target for the development of drugs for the treatment of SLE, and several small molecule SLC15A4 binders have now been reported which are capable of inhibiting TLR7, 8, or 9 signaling. This review summarizes the SLC15A4:TASL complex, its link to SLE, existing evidence for the transporter activity of SLC15A4, the current small molecule binders, and tools available for further drug discovery efforts. - Source: PubMed
Wilkinson Alex LPopat DillonSengmany KathySilva Miguel CCharlton Steven JLay Charles S - Vitamins A and D regulate numerous genes through intersecting metabolic pathways, influencing lung development and asthma. This article aimed to examine the impact of vitamins A and D on lung function, epigenetic ageing and regulatory epigenetics in children and adults with asthma. - Source: PubMed
Publication date: 2026/06/30
Sharma RinkuKachroo PriyadarshiniMendez Kevin MChen QingwenHecker JulianBegum SofinaKelly Rachel SSmith RyanDwaraka VarunCeledon Juan CarlosTantisira Kelan GDeMeo Dawn LWeiss ScottLasky-Su JessicaMcGeachie Michael - Pulmonary fibrosis is driven by maladaptive immune programs that reinforce fibroblast activation. We sought to determine whether profibrotic macrophage states could be therapeutically remodeled to alleviate fibrosis through targeted RNA-based modulation of their intrinsic regulatory circuitry. - Source: PubMed
Publication date: 2026/06/04
Song ZhiminChen JingjingFan JiayingZhang TinghongPeng XingPan YaoZhang YunWang YaofengQin JinlingMeng Shu - 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 - Interferon regulatory factors (IRFs) constitute a family of transcription factors that orchestrate innate and adaptive immune responses, metabolic regulation, and cellular homeostasis. Emerging evidence demonstrates that IRF1-IRF9 play central immunometabolic roles in the formation, progression, and destabilization of atherosclerotic lesions. Pro-inflammatory IRFs, particularly IRF1, IRF3, IRF5, and IRF7, promote endothelial activation, M1 macrophage polarization, pyroptosis, impaired efferocytosis, and maladaptive phenotypic transformation of vascular smooth muscle cells (VSMCs), thereby amplifying vascular inflammation and leading to plaque vulnerability. In contrast, IRF2 and IRF4 exhibit anti-inflammatory and immunoregulatory properties, restraining excessive interferon signaling, supporting M2 macrophage polarization, and maintaining Treg/Th2 homeostasis. IRF8 and IRF9 display highly context- and cell-specific functions, integrating Dendritic cells (DCs) antigen presentation, T-cell activation, and VSMC remodeling with systemic metabolic cues. Therapeutically, both direct and indirect targeting strategies for IRFs are emerging, including small-molecule inhibitors, epigenetic modulators, upstream pathway blockade, microRNA-based interventions, and nutraceutical approaches. However, given their essential roles in antiviral immunity, future translational efforts must prioritize cell-and tissue-specific IRF modulation strategies to prevent systemic immunosuppression. Collectively, IRFs represent a convergent molecular axis linking immune activation, metabolic disturbance, and hemodynamic stress. A deeper understanding of IRF signaling networks, guided by single-cell multi-omics, genetic stratification, and precision delivery systems, may enable the development of immune-metabolic therapies to address residual inflammatory risk in atherosclerotic cardiovascular diseases. - Source: PubMed
Publication date: 2026/06/09
Huang JieWang JiaChen HongGuo FuqiangYuan Xiaofan