Ask about this productRelated genes to: STAT2 antibody
- 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: STAT2 antibody
Related articles to: STAT2 antibody
- Despite the establishment of combined local and systemic therapy as the standard approach for advanced hepatocellular carcinoma (HCC) with portal vein tumor thrombus (PVTT), its efficacy remains constrained by two primary challenges: the immunosuppressive tumor microenvironment (TME) and treatment resistance. Recent research shows that factor Xa (FXa) boosts programmed death-ligand 1 (PD-L1) expression in tumor cells via the proteinase-activated receptor-2 (PAR-2) and signal transducer and activator of transcription 2 (STAT2) pathways, aiding immune evasion. Rivaroxaban, an FXa inhibitor, prevents portal vein thrombosis and disrupts the FXa/PAR-2/PD-L1 axis, restoring T cell function. Based on this mechanism, we propose that incorporating rivaroxaban as a core adjuvant into a long-term, 'local-targeted-immune' multimodal strategy can spatiotemporally reprogram the TME in advanced HCC with PVTT. This approach has the potential to effectively overcome treatment resistance and achieve sustained disease control. The hypothesis is readily testable in clinical trials, and if substantiated, it could establish a new treatment paradigm aimed at improving the prognosis for this high-risk patient population. Furthermore, it would provide a robust theoretical rationale and practical guidance for advancing the treatment of advanced HCC with PVTT. - Source: PubMed
Publication date: 2026/04/27
Yan YingZou DanLi YifanMa HuanhuanChen Hao - Zuo et al. identified a novel post-translational modification-protein pyruvylation-and revealed that pyruvate, a glycolysis metabolite, induces STAT1 pyruvylation at Lys201, which blocks signal transducer and activator of transcription 1 (STAT1)-signal transducer and activator of transcription 2 (STAT2) binding to suppress type I interferon signaling and antiviral immunity. This study provides new insights into antiviral therapy for patients with metabolic diseases. - Source: PubMed
Publication date: 2026/04/20
Yang SongGong LiliLiu Lihong - Mutations in platelet-derived growth factor receptor beta (PDGFRb) cause Kosaki overgrowth syndrome (KOGS). Patients exhibit increased linear growth, craniosynostosis, and thin skin with increased elasticity and scarring. Of the KOGS patients identified to date, three unrelated individuals carried a P584R mutation in the juxtamembrane domain of PDGFRb, resulting in constitutive receptor activation. Due to the limited number of patients, extensive phenotyping and exploration of the molecular basis of disease, including modifier genes, has not been completed. We generated conditional knock-in mice to express mouse PDGFRb with a P583R mutation, corresponding to human P584R, under control of the endogenous Pdgfrb gene. Mutant mice were born at the expected ratio and appeared normal at birth. At 3 weeks of age, mutants began to exhibit connective tissue changes: increased body weight and bone length, craniosynostosis, ectopic bone in the tail and tendons, thin lipodystrophic skin, and high incidence of penile and rectal prolapse. To identify signaling changes caused by mutant PDGFRb signaling, we performed western blotting and phosphoproteomics on dermal fibroblasts. This uncovered increased phosphorylation of PDGFRb, PLCg, Akt1, Shp2, STAT1, STAT2, STAT3, and STAT5. Analysis of 6,621 proteins and 5,386 phosphopeptides identified upregulation of interferon signaling genes linked to STAT1. In many cell types, STAT1 has tumor-suppressor functions and acts to inhibit cell cycle. We generated Stat1-/- Pdgfrb+/P583R mice to test the contribution of STAT1 to KOGS phenotypes. Stat1-deletion exacerbated overgrowth and calvaria dysmorphogensis, and caused keloid-like skin fibrosis. No phenotypes present in the original Pdgfrb+/P583R mice were reverted to normal after Stat1 deletion. Therefore, the P583R mouse model mirrored KOGS phenotypes and increased activation of multiple PDGFRb signaling mediators; in this context, STAT1 activity opposes PDGFRb-driven overgrowth and fibrosis. - Source: PubMed
Publication date: 2026/04/12
Kim JangKwon Hae RyongBerry WilliamOlson Lorin E - Cytotoxic CD8 T lymphocytes are crucial in antiviral immune responses. However, their recruitment to infection sites renders them at risk of viral infection, which could affect their effector activity. CD8 T lymphocytes express RIG-I, which detects cytosolic viral RNA and subsequently induces antiviral gene expression. We investigated how Influenza A virus infection and synthetic triphosphorylated double-stranded RNA, a specific RIG-I ligand, influence TCR-dependent effector responses in primary human CD8 T cells. Cells were isolated from healthy donors and either infected with the reassortant virus RG-PR8-Brazil78 (H1N1) or transfected with the synthetic RNA. Proliferation, degranulation, and cytokine production upon anti-CD3/CD28 stimulation were assessed using flow cytometry and intracellular cytokine staining. Type I IFN production and downstream signaling were measured using IFN-I reporter assay and Western blotting. CRISPR/Cas9 gene editing was employed to knock out RIG-I and STAT2 to evaluate their roles in antiviral responses. Influenza A virus infection of CD8 T cells stimulated RIG-I and activated downstream pathways, including TBK1 and NF-κB, resulting in type-I interferon secretion. Transfection of cytotoxic CD8 T lymphocytes with synthetic RIG-I ligands not only stimulated these pathways but also enhanced the proliferation of CD8 T cells in vitro and protected them from influenza A virus infection. In line with a positive effect on CD8 effector function, both influenza A virus infection and RIG-I ligand transfection enhanced CD8 T cell degranulation and cytokine secretion. Conversely, activation of CD8 T lymphocytes via CD3/CD28 crosslinking increased their susceptibility to influenza A virus infection. We demonstrated that RIG-I stimulation by virus infection or RIG-I ligand transfection promotes intrinsic antiviral pathways and enhances CD8 T-cell effector functions and proliferation. This suggests that RIG-I agonists could enhance and prolong the effector function of cytotoxic CD8 T lymphocytes in immunotherapy. - Source: PubMed
Publication date: 2026/03/27
Mohamed Adham AbuelolaWallerath ChristinaHunkler CharlotteHartmann GuntherStankovic SandaBrooks Andrew GSchlee Martin - - Source: PubMed
Publication date: 2026/04/11
Li KangliZhu BoningWang ShuoZhang XiangleWen XiaodanCao WeijunZhu GuoliangZheng HaixueYang FanZhu Zixiang