STAT2 TAD in vivo Kinase Assay Kit
- Known as:
- STAT2 TAD vivo Kinase Assay Kit
- Catalog number:
- LK0018
- Product Quantity:
- 10ug
- Category:
- Peptides
- Supplier:
- Panomics
- Gene target:
- STAT2 TAD vivo Kinase Assay Kit
Related genes to: STAT2 TAD in vivo Kinase Assay Kit
- 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
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- 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 - Liver zonation is fundamental to hepatic physiology. The zonal loss of Kit in liver sinusoidal endothelial cells (LSECs) during MASH suggests a role in niche maintenance, but its regulatory function is unclear. This study aimed to define how the zonated LSEC Kit controls macrophage distribution in MASH. - Source: PubMed
Publication date: 2026/08/03
Sun LinYue ZhenshengFang ZhiqiangXu HaoDu WeiLing YuweiLiu JingjingSong PingHe FeiDuan JuanliWang Lin - 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 - - Source: PubMed
Publication date: 2026/07/31
Wang MengQiao LiJin LiChen YuanyuanWen XingWang Haijuan - 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