ISGF EMSA Probe Set
- Known as:
- ISGF EMSA Probe Set
- Catalog number:
- AY1333P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- ISGF EMSA Probe Set
Related genes to: ISGF EMSA Probe Set
- Gene:
- IRF9 NIH gene
- Name:
- interferon regulatory factor 9
- Previous symbol:
- ISGF3G
- Synonyms:
- -
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-21
- Date modifiied:
- 2016-10-05
- Gene:
- STAT1 NIH gene
- Name:
- signal transducer and activator of transcription 1
- Previous symbol:
- -
- Synonyms:
- STAT91, ISGF-3
- Chromosome:
- 2q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: ISGF 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: ISGF EMSA Probe Set
- Resistance to inhibitors (BRAFi), alone or with MEK inhibitors (MEKi), limits durable responses in -mutant melanoma. To characterize resistance-associated cell-state evolution, we analyzed 674 melanoma cells from six mice bearing tumors from a single patient-derived V600E-mutant melanoma xenograft (PDX) lineage before treatment, during initial regression, at minimal residual disease, and at resistant regrowth. Unsupervised clustering based on a -centered network feature set comprising 2506 candidate genes identified six transcriptional states, which were characterized using transcriptomic analyses. Cluster 4 was detected exclusively at resistant regrowth, a phase marked by MAPK pathway reactivation, and exhibited enhanced JAK-STAT/interferon signaling and increased , , , , and regulon activities. Network inference predicted - and - regulatory links, suggesting candidate routes to MAPK reactivation through overexpression and -mediated bypass signaling. External analyses partially recapitulated the resistance-associated transcriptional program in independent melanoma cell-line datasets and yielded limited, inconclusive evidence for the predicted - association in public perturbation datasets. Cluster 2 represented a pre-existing proliferative state whose signature was associated with shorter progression-free survival in pretreatment clinical cohorts. Together, these findings distinguish a therapy-associated acquired-resistance state from a pre-existing proliferative resistance-associated state and nominate the predicted - and - links for functional validation. - Source: PubMed
Publication date: 2026/09/09
Fu HaoWang MengyaoZhu HaiboLi WeihuaShen XiaopeiYan HaidanHe Jun - This study aimed to investigate the testicular injury induced by PM2.5 and the associated enhancement of NLRP3/caspase-1/GSDMD-related pyroptotic signaling in rats by integrating animal experiments with public transcriptomic analysis. - Source: PubMed
Publication date: 2026/09/15
Luo YiWang CaoTian MengxiLang GuangyouLi KaixinZhang ZhongyanChu YuXiao QingHong Ma - Apolipoprotein L1 () genetic variants associated with kidney disease become pathogenic when gene expression is induced to high levels; however, the mechanism of gene regulation is not well characterized. Using human podocyte cell lines, the induction of gene expression from various pathogen pattern recognition receptors was universally blocked with a soluble receptor for type I interferons, indicating induction from these different innate immune mechanisms was secondary to autocrine production of type I interferon. Assay for transposase-accessible chromatin sequencing (ATAC-seq) and chromatin immunoprecipitations identified that the gene is regulated by an ISRE-containing promoter and an intronic enhancer containing an interferon-γ activation sequence (GAS) element, which explains its responsiveness to both type I and type II interferons. RNAi-mediated gene silencing identified that the transcription factor required for basal expression levels (IRF1) was not required for interferon-induced expression, which utilized additional transcription factors known to mediate interferon receptor signaling (IRF9 and STATs). An inhibitor of Janus Kinases (JAK), which activates signaling from interferon receptors, was able to attenuate the interferon-induced, but not basal levels of expression. These differential gene regulatory mechanism may be useful in optimizing treatment strategies for APOL1-mediated kidney disease. APOL1 kidney disease is triggered by events that induce high levels of expression. We show here that basal and induced expression are regulated by different mechanisms, with induced expression largely dependent on interferon signaling. Treatment strategies may be developed to selectively block the pathogenic-induced levels of APOL1 while preserving basal levels that are known to provide beneficial functions against parasitic infections. - Source: PubMed
Publication date: 2026/09/14
Huang ChunfaWu ZhenzhenBartolomeo Korey RO'Toole John FSedor John RBruggeman Leslie A - Aging is known to alter innate immune function, increasing susceptibility to viral infections, yet its specific effects on influenza B virus (IBV) infection remain poorly characterized. To address this gap, we developed a preclinical mouse model using a clinically relevant IBV strain Inf B/Phuket/3073/2013 to compare innate immune responses between young adult and aged mice, with a particular focus on age-related transcriptional and proteomic alterations in lung during infection. Bulk RNA sequencing and proteomics analysis of lung tissue harvested post-infection revealed distinct age-dependent transcriptional profiles. Bulk RNA-seq analysis identified 1,350 differentially expressed genes (DEGs), of which 824 exhibited an aged-biased expression pattern and were significantly upregulated in the lungs of influenza B virus-infected aged mice. Functional enrichment of these DEGs indicated perturbations in innate immune signaling, apoptosis, and pathways related to cellular stress and DNA damage in aged mice. There are several differentially expressed proteins that have been identified in young adult and aged influenza B infection. Among these differentially expressed proteins, some commonly co-expressed proteins have a role in virus entry, signaling pathways, and interferon response. Real-time PCR analysis confirmed altered expression of key innate immune genes, including Toll-like receptors (TLRs), interferon regulatory factors (IRF7 and IRF9), key antiviral genes (IFIT -2, IFIT-3 and STAT-1) and type I and II interferons (IFN-α, IFN-β, IFN-γ). Notably, young adult mice exhibited a more coordinated and robust activation of antiviral pathways, whereas aged mice demonstrated delayed and aberrant immune responses, characterized by excessive inflammation and impaired interferon signaling. - Source: PubMed
Publication date: 2026/08/19
Saxena ShikhaKaur GurleenVishwakarma PreetiKumar VarunKumar AmitOmpal SoniaKumar SatishSingh SarjeetChauhan AkankshaChaudhuri SusmitaMalla Waseem AkramSamal Sweety - Mammalian reovirus µ2 antagonizes type I interferon (IFN) signaling and is associated with nuclear hyperaccumulation of IRF9. We tested whether µ2 residue 208, which determines strain-specific IFN-β repression and modulation of host cell mRNA splicing, also controls IRF9 relocalization and whether the splicing factor SRSF2 is required. Recombinant and mutant viruses showed that T1L-like Pro208 is required and sufficient for IRF9 nuclear accumulation in L929 cells. In addition, SRSF2 depletion reduced IFN-mediated induction of and , but not , and abolished T3D-S208P-induced IRF9 nuclear accumulation. Thus, reovirus-induced IRF9 relocalization requires both µ2 residue 208 and host SRSF2. - Source: PubMed
Publication date: 2026/07/27
Rivera-Serrano Efraín E