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
- 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 - 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 - Japanese encephalitis virus (JEV) is a major cause of viral encephalitis and is associated with severe neuroinflammation and neurological damage. Despite extensive research on viral and host determinants of JEV pathogenesis, the influence of environmental factors on disease outcomes remains largely unexplored. This study investigated the impact of Cadmium (Cd), a ubiquitous and persistent environmental heavy metal exposure on JEV infection using in vitro and ex vivo approaches. The findings demonstrate that Cd pre-exposure markedly enhances viral infection, whereas co-exposure and post-exposure have minimal effects on viral infection. Mechanistically, Cd pre-exposure significantly suppressed key virus induced components of the innate antiviral response. Specifically, reduced activation of RIG-I led to the downregulation of TBK1 phosphorylation, which subsequently impaired IRF3 phosphorylation. This attenuation further resulted in decreased expression of STAT1 and STAT2, indicating disruption of downstream interferon signaling. Consistently, the expression of antiviral and inflammatory mediators, including TNF-α, IRF9, and ISG15, was markedly reduced. In contrast, ATF3, a known negative regulator of immune signaling, was significantly upregulated, suggesting its potential involvement in Cd-mediated suppression of antiviral immunity. Together, these results indicate that Cd does not directly enhance viral infection, but instead conditions host cells into an immunologically permissive state prior to infection. This toxicant-induced impairment of innate immunity creates a cellular environment that favours viral establishment and propagation. This study identifies environmental Cd exposure as an important modulator of antiviral immunity and provides insight into how toxicant-induced immune dysregulation can influence viral pathogenesis. - Source: PubMed
Publication date: 2026/07/31
Rawat YogitaGarg ManikaSood VikasKrishnan AnujaKamthan Mohan - Interstitial lung disease (ILD) is a common but serious extra-articular manifestation of rheumatoid arthritis (RA). RA-associated ILD (RA-ILD), which often presents with the usual interstitial pneumonia (UIP) pattern, can resemble idiopathic pulmonary fibrosis (IPF), though the treatment and progression of these two conditions differ. However, the immunologic and molecular mechanisms associated with RA-ILD and IPF development have not been well elucidated at the single-cell level. - Source: PubMed
Publication date: 2026/07/28
Kim DongjunLee HyunKim Sang-HeonEun YeongheeKim Hyun JeKim Bo-Guen