STAT1 Antibody (Phospho-Ser727), pAb, Rabbit
- Known as:
- STAT1 Antibody (Phospho-Ser727), pAb, Rabbit
- Catalog number:
- A00347-100
- Product Quantity:
- 100,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- STAT1 Antibody (Phospho-Ser727) pAb Rabbit
Related genes to: STAT1 Antibody (Phospho-Ser727), pAb, Rabbit
- 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 Antibody (Phospho-Ser727), pAb, Rabbit
Related articles to: STAT1 Antibody (Phospho-Ser727), pAb, Rabbit
- 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 - Porcine deltacoronavirus (PDCoV) is an emerging enteric coronavirus that causes substantial morbidity in swine and may pose a zoonotic risk because of its cross-species transmission potential. Type I interferon (IFN-I) signaling is central to antiviral defense, initiated through the mitochondrial antiviral signaling (MAVS)-TBK1-IFN regulatory factor 3 (IRF3) axis and executed by the downstream JAK-STAT1-STAT2-IRF9 (ISGF3) pathway; however, how PDCoV circumvents both the induction and effector arms of this cascade remains incompletely understood. Here, we identify PDCoV nonstructural protein 13 (Nsp13) as a potent antagonist of IFN-I responses. Ectopic expression of Nsp13 markedly reduces IFN-β production and the expression of IFN-stimulated genes (ISGs, such as ISG56 and CXCL10). Mechanistically, Nsp13 directly binds the C-terminal domain (CTD) of TBK1 and competitively disrupts TBK1 interactions with IRF3 and MAVS. In addition, Nsp13 preferentially binds IRF9 and impairs its nuclear translocation, thereby inhibiting IFN-α-induced signaling. Notably, PDCoV Nsp13 exhibits a host-target binding profile similar to that of SARS-CoV-2 Nsp13, yet it does not alter TBK1 ubiquitination or protein stability. Collectively, these findings reveal a dual-layer immune evasion strategy whereby PDCoV Nsp13 suppresses both IFN induction and downstream signaling, and highlighting Nsp13 as a potential target for antiviral intervention. - Source: PubMed
Wang YingLan ShijinFang ZhenghuiYang ShixingWang XiaochunShen QuanLiu YuweiWu PingZhou ChenglinZhang WenJi Likai - Nasopharyngeal carcinoma (NPC) is an immune-rich epithelial malignancy with marked malignant-cell heterogeneity and variable benefit from immune checkpoint blockade. - Source: PubMed
Publication date: 2026/07/17
Dong LunYao MingzheGao Xiaoping - Sickle cell disease (SCD) is characterized by chronic inflammation and immune dysfunction, yet the underlying signaling defects and their relationship with cellular and systemic immune profiles remain incompletely understood, particularly across different genotypes (HbSS vs HbSC) in pediatric populations. This study characterized the immune landscape in children with SCD. We conducted a case-control study with 53 children with SCD (HbSS and HbSC genotypes) and 27 healthy children with the HbAA genotype. The phenotypes of T helper cells and the phosphorylation status of their STAT proteins were characterised using flow cytometry. Cytokine levels in systemic circulation were quantified using Sandwich ELISA. Children with the HbSC genotype showed significant reductions in CD4TbetIFN-γ (Th1) and CD4Foxp3IL-10 (Treg) cell populations compared to healthy controls. SCD patients exhibited low activation of STAT1, STAT2, STAT4, STAT5, and STAT6 pathways, along with decreased circulating levels of IL-1β, IL-6, TNF-α, IFN-γ, and IL-10. In contrast, IL-17A (Th17) and IL-5 (Th2) levels did not differ between groups. In untreated pediatric SCD, we observed STAT downregulation, Th1/Treg deficits, and decreased IL-1β, TNF-α, IL-6, IFN-γ, and IL-10, with preserved Th2/Th17 responses. HbSS and HbSC showed minimal differences, suggesting a shared impairment of the STAT-Th1-IFN-γ axis. - Source: PubMed
Publication date: 2026/07/14
Mazou BassimtouKatawa GnatoulmaBara Fagdéba DavidTchadie Edlom PélagieGnodja TégmabaMagnang HèzouwèKolou MaléwéRitter Manuel