IRF1 _ IRF2 EMSA Kit
- Known as:
- IRF1 _ IRF2 EMSA Kit
- Catalog number:
- AY1115
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- IRF1 _ IRF2 EMSA Kit
Related genes to: IRF1 _ IRF2 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
- 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
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- 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 - The innate immune cGAS-STING-IRF3-IFN signaling pathway plays a crucial role in host antiviral defense. While mammalian IRF families encompass IRF1 through IRF9, the involvement of IRF members other than IRF3 in cGAS-STING antiviral signaling transduction and/or regulation remains poorly characterized. Through dual screening systems, we identified the porcine (p) IRF2 as a potent suppressor of porcine cGAS-STING-IFN antiviral signaling. First, we demonstrate that pIRF2 suppresses both cGAS-STING- and TBK1/IKKε/IRF3-activated IFN signaling. Further, we reveal that pIRF2 does not affect STING-activated IRF3 phosphorylation, nor does it impair IRF3 dimerization or nuclear translocation. The inhibitory activity of pIRF2 depends on its DNA binding domain (DBD) but not IRF-associated domain (IAD). Importantly, we find that pIRF2 directly binds the IFN-β promoter and competes IRF3 for binding to IFN-β promoter. In summary, our findings unveil a distinct function of pIRF2 as well as the regulatory mechanism governing porcine cGAS-STING-IFN antiviral function. - Source: PubMed
Publication date: 2026/02/10
Jiang SenHe JingyuWang KunLv MengjiaXia NengwenJiao JunChen NanhuaZheng WanglongZhu Jianzhong - Coronaviruses, members of the betacoronavirus genus. They are mostly enveloped and has +ve sense RNA which infects a wide range of hosts, including mammals and birds. This SARS-CoV-2 in December 2019 triggered a global pandemic, with transmission primarily occurring through respiratory droplets. SARS-CoV-2 comprises four structural proteins namely: spike, membrane, envelope and nucleocapsid protein (S, M, E, and N respectively) along with multiple non-structural proteins (nsp1-nsp16) essential for infections. The trimeric S protein, composed of S1 and S2 subunits which helps in virus entry into the cell after attachment to the ACE2 recpetor of host cell. Interferon regulatory factors (IRF-1 and IRF-2) are critical transcription factors in antiviral immune responses, yet their specific roles in SARS-CoV-2 infection remain insufficiently understood. Disruption of their regulatory functions may compromise host antiviral defenses and influence disease progression. Elucidating the mechanistic roles of IRF-1 and IRF-2 could facilitate the production of novel therapeutic strategies which further modulates the immune responses, mitigates the viral pathogenicity, and hence clinical outcomes will be improved. A deep insight of these immune pathways is pivotal for designing targeted interventions to strengthen host resilience against coronavirus infections. - Source: PubMed
Singh EktaNishi NishitaTripathi MuditaPrakash Krishna - Interferon regulatory factors (IRFs) play key roles during viral and bacterial infections. However, their regulation by inflammatory cytokines, including interleukin (IL)-1β and tumor necrosis factor (TNF) α, remains underexplored. As airway epithelial cells (AECs) modulate lung inflammation, IRF expression was characterized in pulmonary A549 and bronchial BEAS-2B epithelial cells along with primary AECs grown in submersion, or air-liquid interface, culture. While, IRF6 mRNA was only highly expressed in primary cells, IRF4 and IRF8 mRNAs were consistently low across the models. All the other IRF mRNAs were expressed in each model. IRF3 and IRF9 mRNAs were highly expressed, but their proteins remained primarily cytoplasmic post-IL-1β treatment in A549 cells. IRF2 showed moderate/high mRNA expression and was constitutively nuclear. However, RNA silencing did not support roles for IRF2 or IRF3, with only a modest role for IRF9, in the IL-1β-induced activation of an IRF reporter. IRF1 mRNA was highly induced by IL-1β in A549 and primary cells. Similarly, IRF1 protein was increased by IL-1β and TNFα in A549 cells, and by TNFα in BEAS-2B cells. In A549 cells, IL-1β-induced IRF1 protein localized to the nucleus and since IRF1 silencing prevented IRF reporter activity, a major transcriptional role was indicated. Mechanistically, the inflammatory transcription factor, nuclear factor (NF)-κB, was necessary for IL-1β- and TNFα-induced IRF1 expression. Further, four novel enhancer regions 5' to IRF1 bound the NF-κB subunit, p65, and their IL-1β/TNFα-induced reporter activity required consensus NF-κB motifs. Three such regions recruited RNA polymerase-2 and were flanked by the active chromatin mark, histone 3 lysine 27 acetylation, supporting enhancer involvement in IRF1 transcription. Finally, IRF1 expression, transcription rate, and enhancer activity induced by IL-1β, or TNFα, were relatively unaffected by glucocorticoid. IRF1-dependent gene expression may therefore show insensitivity to glucocorticoid and could contribute to glucocorticoid-resistance in diseases that include severe asthma. - Source: PubMed
Publication date: 2025/12/08
Necker-Brown AmandahMostafa Mahmoud MGeorgescu AndreiThorne Andrew JChandramohan PriyankaKooi CoraKalyanaraman KeerthanaGao AlexBansal AkankshaSasse Sarah KGerber Anthony NLeigh RichardNewton Robert