STAT1 CMV Expression Vector
- Known as:
- STAT1 cytomegalovirus Expression Vector
- Catalog number:
- ME0033
- Product Quantity:
- 15 ug
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- STAT1 CMV Expression Vector
Related genes to: STAT1 CMV Expression Vector
- 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
- Gene:
- STAT2 NIH gene
- Name:
- signal transducer and activator of transcription 2
- Previous symbol:
- -
- Synonyms:
- STAT113
- Chromosome:
- 12q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-08
- Date modifiied:
- 2019-04-23
Related products to: STAT1 CMV Expression Vector
Related articles to: STAT1 CMV Expression Vector
- Nipah virus (NiV) is a highly lethal zoonotic paramyxovirus harbored by fruit bats (Pteropodidae). The virus spreads through zoonotic spillover via intermediate animal hosts or contaminated environments, and through human-to-human transmission. Since its emergence in 1998, NiV has triggered recurrent outbreaks across South and Southeast Asia, with case-fatality rates of 40-75%. Two genotypes (NiV-M and NiV-B) differ in transmissibility and pathogenicity. WHO-listed as a priority pathogen, NiV has no approved vaccines or antiviral therapeutics. The virus gains entry into host cells through Ephrin-B2/B3 receptors, and evades innate immunity via non-structural proteins (V, W, C) and structural proteins. These evasion strategies disrupt multiple nodes in type I and II interferon (IFN-I/II) signaling pathways, including suppression of RIG-I/MAVS and inhibition of STAT1/STAT2 nuclear translocation, and dysregulation of NF-κB activation. Finally, these mechanisms facilitate viral replication and systemic dissemination. Infection also elicits adaptive immunity, including neutralizing antibodies against viral glycoproteins (G and F) and durable virus-specific CD4⁺ and CD8⁺ T-cell responses. Fatal outcomes correlate with high early viremia, delayed or insufficient antibody production, and dysregulated innate and adaptive immunity. In affected organs, particularly the brain, persistent cytokine storm driven predominantly by CXCL10 recruits inflammatory infiltrates and amplifies immunopathological damage. Current intervention strategies include vaccine candidates (ChAdOx1 Nipah B, mRNA-1215, HeV-sG) and antiviral approaches such as nucleoside analogs, monoclonal antibodies, and fusion inhibitors. This review comprehensively synthesizes current knowledge on NiV epidemiology, pathogenesis, and countermeasure development, providing a conceptual framework to interpret its exceptional virulence and prioritize targets for effective outbreak control. - Source: PubMed
Publication date: 2026/08/31
Sun HaoYuan XinLi JinyanLi XitangJin YuefeiDuan Guangcai - Inflammatory bowel disease is characterized by unresolved mucosal inflammation driven mainly by TNFα and/or interferon gamma (IFNγ). While anti-TNFα biologics are a clinical mainstay, therapeutic resistance remains a significant hurdle. The molecular mechanisms that sustain inflammation in anti-TNFα nonresponders are not fully understood. In human colon biopsies, we identified significant upregulation of the deubiquitinase OTUD5 in nonresponders compared to responders, suggesting its involvement in therapy resistance. Using an intestinal epithelial cell -specific Otud5 KO mouse model, we show that Otud5 deficiency significantly alleviated the IFNγ-dependent colitis induced by dextran sulfate sodium, as evidenced by reduced weight loss and diminished infiltration of Ly6C inflammatory monocytes. Mechanistically, IFNγ induces OTUD5 expression through a nontranscriptional mechanism; in turn, OTUD5 stabilizes STAT1 and STAT2 by preventing their ubiquitination and subsequent degradation. This sustains IFNγ-ISGF3 signaling, which directly drives the expression of CCL8, a critical chemokine for monocyte recruitment. Targeting this pathway with a newly identified small-molecule inhibitor, CT1170, which exhibits potent activity against OTUD5, blocked the IFNγ-ISGF3-CCL8 axis, halted colitis progression, and suppressed colitis-elicited tumorigenesis. These findings were validated in human inflammatory bowel disease organoids, where CT1170 effectively disrupted IFNγ-driven inflammatory signaling. - Source: PubMed
Publication date: 2026/08/13
Guan HuiyuanCai ChangzhouWang JieweiLiu ZhaoxuePeng JinBai XupengWu LingzhiJiang KunZhen XinghuaYu ChaohuiZhang PuminShen Zhe - Rheumatoid arthritis (RA) is driven in part by hyperactivated fibroblast-like synoviocytes (FLS) that invade articular structures. Iguratimod (IGU), a conventional synthetic DMARD, is clinically effective, but its direct molecular target and impact on synovial cell-cell crosstalk remain unclear. We aimed to elucidate how IGU regulates FLS invasiveness and inflammatory signaling, identify its upstream target within the JAK-STAT pathway, and develop a prodrug with improved pharmacokinetics while preserving disease-modifying activity. - Source: PubMed
Publication date: 2026/08/03
Tao LinJiang WenHuang YulangFu XuefengWang HanYang HelinLi HaoTian ZixuanLiu DanWang ShaojieZhu Yue - The mechanisms sustaining chronic inflammation in rheumatoid arthritis (RA) remain incompletely understood. Here we show that branched-chain amino acid (BCAA) catabolism, mediated by the mitochondrial enzyme BCAT2, sustained interferon-driven macrophage activation in autoimmune arthritis. Multi-omics and histological analyses of individuals with active RA or sustained remission revealed that active disease was associated with systemic BCAA depletion, synovial branched-chain ketoacid accumulation and elevated BCAT2 expression in interferon-responsive synovial macrophages. Mechanistically, interferon-γ induced BCAT2 transcription through the transcription factor IRF1 in RA synovial macrophages. In human monocyte-derived macrophages, BCAT2-dependent BCAA catabolism elevated mitochondrial reactive oxygen species, which in turn restrained SHP-1 activity, prolonged STAT1 and STAT2 phosphorylation and drove inflammatory cytokine production. Furthermore, myeloid-specific deletion of Bcat2 ameliorated collagen antibody-induced arthritis in mice. Pharmacological targeting of this pathway with telmisartan suppressed persistent arthritis in methotrexate-treated mice. Together, our findings identified BCAT2-dependent amino acid catabolism as a potentially targetable metabolic pathway in autoimmune arthritis. - Source: PubMed
Publication date: 2026/07/31
Meng XiaohuiHan HaihuiYou WulinXin PengfeiJu YaCai LiangyuZhou LameiZhong ShengHu ZhuoyiChen ZhiyuQin WenleiGe YanhaoYao WeiXiao LianboZhang Yafeng - 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