IRF1 EMSA Probe Set
- Known as:
- IRF1 EMSA Probe Set
- Catalog number:
- AY1021P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- IRF1 EMSA Probe Set
Related genes to: IRF1 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
Related products to: IRF1 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 EMSA Probe Set
- Atopic dermatitis (AD) is a persistent skin disorder involving inflammation and marked by immune dysregulation. Sinomenine, a plant-derived alkaloid with known anti-inflammatory properties, remains underexplored regarding its role in pyroptosis associated with AD. An in vitro AD-like model was established using HaCaT cells stimulated with IFN-γ (10 ng/mL) and TNF-α (10 ng/mL). Sinomenine pretreatment was evaluated for its ability to attenuate inflammation, pyroptosis, and cell damage using ELISA, MTT, LDH assays, flow cytometry, and Western blot. The underlying mechanism was explored via ChIP-qPCR, luciferase assays, and protein interaction studies including co-immunoprecipitation and immunofluorescence. IFN-γ/TNF-α triggered robust pyroptosis in HaCaT cells, characterized by elevated IL-18, IL-6, IL-8, IL-1β, and increased NLRP3 expression levels, cleaved Caspase-1, and GSDMD-N. Sinomenine pretreatment significantly reversed these effects, improving cell viability and reducing inflammatory cytokine production and pyroptosis markers. Mechanistically, sinomenine downregulated TRAF6 expression, a known activator of the NLRP3 inflammasome, by inhibiting its transcriptional regulator IRF1. IRF1 directly bound the TRAF6 promoter and promoted its transcription. Furthermore, sinomenine enhanced TRIM32 expression, which promoted the ubiquitination and proteasomal degradation of IRF1, thus interrupting the IRF1/TRAF6/NLRP3 axis. Sinomenine protects HaCaT cells from IFN-γ/TNF-α-induced pyroptosis by promoting TRIM32-mediated degradation of IRF1, leading to downregulation of TRAF6 and subsequent attenuation of the NLRP3 inflammasome activation. These findings highlight the therapeutic potential of sinomenine for inflammatory skin diseases like AD. - Source: PubMed
Xia JieLiu YongBai QiGong KeLiu YingTan ZhichenLuo JiaZhu Mingfang - B cells are highly abundant lymphocytes and central players in humoral immunity. Although T cells are well known to support humoral responses, how B cells influence T cell responses is less understood. Here, we show that B cells are critical for CD8 T cell responses to chronic, but not acute, viral infections. In the absence of B cells, T cells responding to chronic infection exhibited severely impaired effector differentiation. This dependency on B cell help was dictated by high antigen loads and strong T cell receptor (TCR) stimulation. Loss of either B cells or interferon-I (IFN-I) signaling led to severe functional deficits in exhausted T cells, implicating B cells as key producers of IFN-I. The IFN-I-dependent T cell response to strong TCR stimulation is mediated, in part, by the transcription factor IRF1. Therefore, during chronic infection, we uncover an important role for B cell-derived IFN-I in modulating T cell responses to strong TCR stimulation. - Source: PubMed
Publication date: 2026/07/02
Gago da Graça CatarinaCao YuxiLi SiningLindemann Anna FHeyden LeonieWijesinghe Sharanya K MPoch AnnikaNguyen Minh-Hanh THuynh-Anh Nhat TDaum ElenaChen DanielleTsui CarlsonRupasinghe ErandiGantier Michael PRoers AxelThimme RobertHofmann MaikeBedoui SammyAbdullah ZeinabSchröder JanKallies AxelAlexandre Yannick OUtzschneider Daniel T - 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