STAT1 Antibody
- Known as:
- STAT1 Antibody
- Catalog number:
- XW-8116
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- STAT1 Antibody
Related genes to: STAT1 Antibody
- 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
Related articles to: STAT1 Antibody
- Lymph node metastasis in esophageal squamous cell carcinoma (ESCC) is associated with poor prognosis, and screening for potential biomarkers of metastasis is significant for improving the prognosis of ESCC. After batch effect removal and integration of two ESCC transcriptome datasets (GSE157804, GSE118493), differentially expressioned gene analysis was performed. The intersection of differentially expressed genes was obtained to identify characteristic genes associated with lymph node metastasis in ESCC. GO/KEGG enrichment analyses were conducted for the characteristic genes. The top 10 pathways and pathway genes based on q-value were selected to construct a PPI network. Hub genes were identified and intersected with the characteristic genes to determine key genes. GO/KEGG enrichment, expression level analysis, and immune infiltration analysis were performed for the key genes. Immunohistochemistry was used to validate the expression levels of key genes in clinical samples. A cell model with regulated expression of key genes was established to verify their impact on the invasive and migratory capabilities of ESCC cells and epithelial-mesenchymal transition (EMT), as well as ECM‑related gene expression. A total of 542 characteristic genes associated with lymph node metastasis in ESCC were identified through differential gene analysis, which were mainly enriched in extracellular matrix-related pathways. PPI network analysis identified 63 hub genes, and the intersection with characteristic genes resulted in 20 key genes, which were also primarily enriched in extracellular matrix-related pathways. Expression level analysis showed that key genes such as STAT1, STAT2, IFIT1, and IFIT3 were highly expressed in metastatic ESCC tissues compared to primary sites and adjacent non-tumor tissues. Immune infiltration analysis revealed a significant positive correlation between IFIT3, STAT1, STAT2, and M1 macrophage polarization. Immunohistochemical analysis indicated high expression of STAT1 in ESCC patient samples with lymph node metastasis. Upregulation of STAT1 in ESCC cells enhanced cell invasion, migration, EMT levels and ECM‑related gene expression, while downregulation of STAT1 expression suppressed these processes. Consistently, an additional gain‑of‑function experiment further confirmed these promoting effects. STAT1 serves as a biomarker for lymph node metastasis in ESCC. The expression level of STAT1 is positively correlated with the degree of lymph node metastasis in ESCC clinical samples. Overexpression of STAT1 promotes the invasion, migration, EMT and ECM‑related gene expression of ESCC cells, while the downregulation of STAT1 inhibits these effects. - Source: PubMed
Publication date: 2026/09/05
Lv GuoliLi HaoyuLei YoumingPeng JungaoLiu FanghaoZhao Wei - Immune signaling is tightly coupled to cellular metabolic state. Beyond supplying energy, metabolites can directly regulate immune responses by driving post-translational modifications of proteins and chromatin, shifting immunometabolism toward a model in which metabolic state encodes signaling outputs. - Source: PubMed
Publication date: 2026/08/21
Zhang ZiyeXu MingzeZhang SenZhang ZhikunZhang HongguangWang ZhenjieZhu MinZhao Hongchang - 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