Ask about this productRelated 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
- Mycobacterium bovis bacillus Calmette-Guerin (BCG) is a form of live attenuated M. bovis-based vaccine used to prevent tuberculosis and other mycobacterial infections. BCG immunization also provides cross-protection against a broad range of viral pathogens. Recent studies show that a coordinated induction of innate and adaptive immune responses is involved, though the mechanisms are less defined. To investigate the cross-protection of BCG against virus infection, we used a mouse model of respiratory syncytial virus (RSV) infection and demonstrated that systemic administration of live BCG altered chromatin accessibility for transcriptional factor expression favoring Th1 response. Specifically, BCG-IV immunization protected mice against RSV infection. BCG immunization caused metabolic reprogramming in monocytes and neutrophils and innate immune response, leading to IL12/IL12R-mediated naïve CD4 T cell differentiation to the Th1 cell population. Integrated analysis of chromatin openness and transcriptomic data revealed that BCG administration upregulated transcription factors including interferon regulatory factors (IRF1) and signal transducer and activator of transcription (STAT1 and STAT2), a signature for interferon signaling and antiviral response. This work highlights a crucial role for the adaptive immune response in mediating naïve CD4 T cell differentiation and cross-protection through epigenetic remodeling for antiviral response against pathogens in an antigen-agnostic manner. - Source: PubMed
Publication date: 2026/05/16
Wang RuilinZhao YuanhuiYang JieLuo RenjieSun WeikangZhang MengyuLiu XiangdongHou YayiCao PengLi Erguang - Porcine epidemic diarrhea virus (PEDV) continues to pose a global threat to the swine industry, causing fatal neonatal diarrhea with a mortality rate approaching 100%. Currently, no effective targeted drugs have been approved. The coronavirus main protease (M), a conserved enzyme essential for viral replication, represents a promising target for antiviral development. Here, we demonstrate that Closantel, an FDA-approved veterinary drug, acts as a potent pan-coronavirus M inhibitor via enzymatic inhibition assays. Moreover, Closantel potently suppresses PEDV replication in Vero-E6 and IPEC-J2 cells, with EC values of 1.49 ± 0.38 μM and 4.32 ± 0.53 μM, respectively, and exhibits minimal cytotoxicity. Remarkably, Closantel triggers interferon secretion and activates JAK-STAT signaling pathways via phosphorylation of STAT1 and STAT2, establishing a dual antiviral mechanism. In summary, Closantel holds promise as a potential lead compound for developing targeted therapies against PEDV infection. - Source: PubMed
Publication date: 2026/05/12
Zhang LeiWang ZhuoyaXu FengLin Yuxi - 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 - 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