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
- The development of compounds triggering intestinal stem cells (ISCs) proliferation represents a promising strategy to alleviate irradiation (IR)-induced gastrointestinal syndrome. Here, cannabidiol (CBD)-a nonpsychotomimetic phytocannabinoid derived from the Cannabis sativa plant-was found to dramatically improve body weight loss of mice and stimulate Lgr5 ISCs proliferation upon a lethal dose of IR. Using absolute quantitative lipidomics, we found that the dysregulation of fatty acids in crypts induced by IR was rescued by CBD, which was indispensable for ISCs regeneration. Integrative analysis of transcriptome and lipidomics unveiled the critical role of PPARα in regulating fatty acid β-oxidation (FAO) by transcriptionally upregulating Slc27a2 and Acox1. Further experiments showed that CBD could trigger the enrichment of Stat2 on the promoter region of Pparα, ultimately facilitating the FAO program and subsequent ISCs proliferation following IR exposure. In addition,THOC3 was identified as a direct target of CBD, which stabilized the THOC3 protein and substantially alleviated the IR-induced blockade of Stat2 mRNA nuclear export. This study reveals a connection between CBD-driven ISCs proliferation and the FAO program during IR damage, providing a promising avenue for IR-induced gastrointestinal syndrome treatment. The binding of CBD to THOC3 maintains its radiation stability, which then supports the nuclear export of Stat2 mRNA for the subsequent transactivation of Pparα. The upregulation of PPARα will ultimately stimulate the FAO program, thereby facilitating ISCs regeneration during IR exposure. - Source: PubMed
Publication date: 2026/05/12
Liao ZebinHuang CongshuZhang LiangliangHu ChangkunWu ZekunBai ZhijieLi GaofuZhou LeiWang NingningHuangfu ChaojiNi ZhexinShen PanZhou WeiGao Yue - Natural bioactive polysaccharides have been investigated for their ability to modulate antiviral immune responses. Polysaccharide peptide (PSP) from previously restricted human immunodeficiency virus type 1 (HIV-1) entry into monocytic cells through a protein kinase R (PKR)-dependent cytoskeletal mechanism. However, its impact on antiviral signaling in adaptive cluster of differentiation 4 (CD4)+ T-cell models remains incompletely defined. Here, we evaluated concentration- and time-dependent effects of PSP (50-1000 µg/mL) in Jurkat T cells over 3 and 6 days. Cell viability was assessed by MTT, trypan blue exclusion, and viable cell density analysis. Immunoblotting and reverse transcription quantitative polymerase chain reaction (RT-qPCR) were performed to examine Toll-like receptor 4 (TLR4), nuclear factor kappa B (NF-κB), signal transducer and activator of transcription 1 and 2 (STAT1/STAT2), PKR, interferon gamma (IFN-γ), and cofilin-1 signaling. PSP did not induce cytotoxicity at any concentration. Instead, PSP promoted dose- and time-dependent upregulation of intracellular TLR4, PKR, phospho-PKR (Thr446), Cofilin-1, phospho-Cofilin-1 (Ser3), phospho-STAT1 (Tyr701), phospho-STAT2 (Tyr690), phospho-NF-κB (Ser536), and IFN-γ, with amplified responses at Day 6. These changes were paralleled by transcriptional induction of antiviral-associated genes. Collectively, PSP induces coordinated interferon (IFN)-associated and cytoskeletal regulatory signaling in Jurkat T cells without cytotoxicity, providing a mechanistic framework for future evaluation of viral permissiveness and antiviral responses in adaptive immune models. - Source: PubMed
Publication date: 2026/04/20
Rosario-Sanfiorenzo Glamaris NAlicea-Pérez Giovanni OÁlvarez-Flores Ashlin NHernández-Santisteban Naiara IRivera-Payán Amanda CColón-Fernández Jeshua JRivera-Berganzo Abigail MBermudez-Fosse VictoriaSantana-Costas IleanmarieNieves-Moreno CarolinaColón-Santiago Fabiola ICorrea-Haifa Julieness MSánchez-Otero Natalia ICintrón-Vélez GeraldineMatos-Morales Génesis MÁlvarez-Rivera Eduardo - 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