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
- Porcine circovirus type 3 (PCV3), a newly identified pathogen linked to multiple clinical diseases, threatens the global swine industry. Nucleolin, a multifunctional protein involved in various biological events, has been confirmed to suppresses PCV3 replication; however, the underlying molecular mechanism remains unclear. Herein, we demonstrate that nucleolin inhibits PCV3 replication by activating the type I interferon (IFN)/Janus kinase (JAK)-signal transducer and activator of transcription 1 (STAT1) pathway, a critical host antiviral defense axis. Mechanistically, nucleolin enhances STAT1/STAT2 phosphorylation, promotes their nuclear translocation, and interacts with IFN regulatory factor 9 (IRF9), thereby driving the formation of the IFN-stimulated gene factor 3 (ISGF3) complex and the subsequent production of interferon-stimulated genes (ISGs). Furthermore, PCV3 infection antagonizes JAK-STAT1 activation, an effect that is reversed by nucleolin overexpression. Notably, the JAK-STAT1 pathway agonist RO8191 not only inhibits PCV3 replication in cultured cells but also reduces PCV3 viral load and alleviates PCV3-induced pathological lesions in the lungs and spleens of mice. Collectively, these results indicate that PCV3 facilitates its own replication by suppressing this pathway, whereas nucleolin exerts its antiviral activity by counteracting this suppression, specifically by targeting the STAT1-STAT2-IRF9 signaling axis. - Source: PubMed
Publication date: 2026/10/01
Wang DedongLan XiaoyuanLi JianyiYang XiaoyuShi YongyanZhou JianweiWan JiawuHou LeiLiu Jue - BACKGROUND Alzheimer's disease (AD) is associated with transcriptional dysregulation, but gene-level analyses may overlook isoform changes. We investigated how differential isoform usage, promoter selection, and splicing contribute to transcriptome remodeling in the AD frontal cortex. METHODS We analyzed Oxford Nanopore long-read RNA sequencing data from frontal cortex of six individuals with AD and six controls. Transcripts were quantified using Bambu, and differential isoform usage was assessed using IsoformSwitchAnalyzeR. Promoter usage and SUPPA2-derived percent-spliced-in values were tested using beta regression. Transcription factor motif enrichment was evaluated at differentially used promoters. Transcript-level effects were compared with an independent short-read cohort. RESULTS We identified 109 isoform-switching events involving 96 isoforms across 86 genes, including , , , , and . Several switches altered predicted nonsense-mediated decay sensitivity. Eleven genes exhibited promoter switching, comprising 46 differentially used promoters: 31 with increased and 15 with decreased usage in AD. These promoters were enriched for 179 TF motifs. IRF7, IRF8, IRF9, and STAT1::STAT2 motifs were top-ranked among promoters with increased usage, whereas NFKB1 and NFKB2 motifs were top-ranked among those with decreased usage. Targeted analysis identified 14 significant differential splicing events with sex-associated effects, including . Although cross-platform concordance was weak, 16 of 26 transcripts with large effects in both datasets changed concordantly, and 13 showed large, concordant effects of similar magnitude. CONCLUSIONS AD-associated transcriptome remodeling extends beyond gene-level abundance to include changes in isoform proportions, promoter selection, and transcript structure. These findings implicate transcription initiation and RNA processing as complementary layers of dysregulation in AD. - Source: PubMed
Publication date: 2026/09/13
Aquino JelardLee AliceZheng JenniferKu Wai LimHan MiraChen Jingchun - 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