IRF1 _ IRF2 EMSA Probe Set
- Known as:
- IRF1 _ IRF2 EMSA Probe Set
- Catalog number:
- AY1115P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- IRF1 _ IRF2 EMSA Probe Set
Related genes to: IRF1 _ IRF2 EMSA Probe Set
- 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
- Gene:
- IRF2 NIH gene
- Name:
- interferon regulatory factor 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4q35.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-05-09
- Date modifiied:
- 2016-01-15
Related products to: IRF1 _ IRF2 EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: IRF1 _ IRF2 EMSA Probe Set
- 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 - Multiple myeloma (MM), the second most prevalent hematologic malignancy, remains incurable, highlighting the need to identify molecular drivers of disease progression and new therapies. Using a CRISPR-Cas9 library screening approach in MM cells, we identified 22 essential transcription factors (TFs), including members of the interferon regulatory factor (IRF) family. Remarkably, in addition to the well-known IRF4, IRF2 emerged as a critical TF in MM. Cleavage under targets and release using nuclease (CUT&RUN) experiments demonstrated that IRF2 binds extensively to chromatin, both independently and in cooperation with IRF1 and IRF4. Although IRF2-unique regions were predominantly associated with active promoters, regions bound by IRF2/1/4 were biased toward introns. Functionally, IRF2 contributes to MM cell survival by suppressing necroptosis and promoting cell migration. Notably, IRF2-dependent transcriptional dysregulation was evident in precursor conditions such as monoclonal gammopathy of undetermined significance (MGUS) and smoldering MM (SMM), suggesting a role in early disease evolution. In addition to its role as an early factor, IRF2 levels also seem to influence disease progression, as MMs with higher expression demonstrated worse progression-free survival (PFS) and overall survival (OS) in both univariate and multivariate analyses, even after adjusting for common MM genetic risk factors. In conclusion, IRF2 constitutes an underappreciated essential TF involved in the pathogenesis and clinical behavior of MM. Its inhibition leads to dysregulation of key signaling pathways in MM pathogenesis, highlighting its potential as a therapeutic target. - Source: PubMed
Gómez-Echarte NahiaCarrasco-León ArantxaMaiqués-Díaz AlbaBarrena NaroaMiranda EstibalizGarate LeireAmundarain AneSan Martín-Uriz PatxiCharalampopoulou StellaValcárcel Luis VitoresAriceta BeñatRodriguez-Marquez PaulaRodriguez-Madoz Juan RobertoIshiguro KazuyaPlanes Francisco JRodriguez-Otero PaulaMitsiades Constantine SMartín-Subero José IgnacioSan José-Enériz EdurneProsper FelipeAgirre Xabier - Recent findings emphasize that IRF1 and IRF2 play distinct roles in gene regulation, particularly through chromatin remodeling during antiviral responses. Our current data extend this by revealing that IRF1 directly targets TNS3, a key regulator of renal stress, fibrosis, and the aging process. We identify a mechanistic parallel between the IRF1-TLR3 and IRF1-TNS3 pathways, proposing that targeting the IRF1-mediated modulation of TNS3 could offer a fresh therapeutic approach for kidney injury. - Source: PubMed
Publication date: 2026/03/19
Huang Chien-WeiWen Chen-YuehHsu Yu-JueiLi Chia-Jung - Interferon regulatory factors (IRFs) are essential for transcription of interferons (IFNs), interferon-stimulated genes (ISGs), and pro-inflammatory cytokines. We profile the transcriptome of human monocyte THP1 cells challenged with cGAMP, LPS, or IFNB1 protein as a function of knockout (KO) or overexpression (OE) of IRFs or KO of IFNAR2. We define distinct gene expression groups, reflecting the transcription factors responsible for their induction including subgroups activated by more than one pathway or feed-forward regulation. We compare IRF3- and IRF7-induced gene signatures and note the strong direct induction of a subset of antiviral-acting ISGs by IRF3 or IRF7. LPS treatment induces NF-κB responses in monocyte and macrophage state cells, however, IFNs and ISGs are only co-induced in the macrophage state requiring IRF3. IRF1, IRF2, IRF5, and IRF8 are largely dispensable for IFN-stimulated or innate-immune-mediated gene induction. This study provides a valuable resource for dissecting complex inflammatory gene signatures and their underlying transcription factors thereby anticipating the effects of selectively drugging the underlying pathways. - Source: PubMed
Publication date: 2026/02/12
Lama LodoeMorozov PavelGarzia AitorTuschl Thomas