Ask about this productRelated genes to: STAT5A antibody
- Gene:
- STAT5A NIH gene
- Name:
- signal transducer and activator of transcription 5A
- Previous symbol:
- STAT5
- Synonyms:
- MGF
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-09
- Date modifiied:
- 2016-10-05
Related products to: STAT5A antibody
Related articles to: STAT5A antibody
- To investigate the tumor-intrinsic lymphocyte cytosolic protein 2 (LCP2) in esophageal squamous cell carcinoma (ESCA) and its molecular mechanisms in mediating resistance to programmed death-1 (PD-1) therapy. - Source: PubMed
Publication date: 2026/05/27
Zhang YuanDang YunzhiWang JunZhao BoLi ZhibinWang XinLiang Kun - The Interleukin-6 (IL6)-Interleukin-6 receptor (IL6R)-Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway plays a crucial role in innate immunity by inducing the production of various immune effectors. However, its stepwise evolutionary assembly across metazoans remains incompletely characterized. - Source: PubMed
Publication date: 2026/05/09
Yu HongChang RenleWang HouyouHe MuchunSun JiejieSong Linsheng - Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a common urological condition in men. Although disruption of the Th17 (T helper 17)/Treg (regulatory T) balance has been implicated in its pathogenesis, the upstream drivers of this immune imbalance remain incompletely understood. This study investigated whether interleukin-6 (IL-6) is associated with altered Th17/Treg homeostasis and impaired Treg function in experimental autoimmune prostatitis (EAP). - Source: PubMed
Liu XianhongBian XiaokangHan ShanchuanLi BoyangSong JianLiang ChaozhaoZhou JunChen Xianguo - Insulin signaling regulates cellular metabolism in an epigenetic manner, but its role in the immune cell homeostasis remains unknown. High plasma insulin obstructs efficient insulin signaling and rewires metabolic activity in autoimmunity. In this study, we explored the functional consequences of insulin signaling for the metabolism and phenotype of effector CD4 T cells in blood and synovial tissue of patients with rheumatoid arthritis (RA). Transcriptome profiling of CD4 cells in RA blood and synovia revealed high metabolic activity and effector function of the survivin/BIRC5PD1 T peripheral helper cell population. Low insulin signaling and deficient histone acetylation in RA T cells amplified proinflammatory IFNγ and TNF expression. Co-deposition of survivin with acetylated histone H3K27 on regulatory chromatin controlled the transcription of histone acetylation complex subunits and insulin-dependent genes. Insulin stimulation and histone deacetylase inhibition induced an increase in histone acetylation. In CD4 cell cultures and in aggressive PD1Tph cells in RA synovial tissue, exposure to insulin synergized with inhibition of histone deacetylation to upregulate IL7 production suppressing IFNγ and PD1. This activated IL7R-signaling mediators STAT5A/B, BCL2, and promoted acquisition of CD27CD45RO central memory phenotype in the PD1Tph cells. Likewise, the CD4 cells in hyperinsulinemic T2D patients showed enrichment of IL7RT cell cluster. In RA patients, antagonizing folate transport and JAK/STAT signaling activated insulin signaling and histone acetylation-dependent metabolism of CD4 cells. Concomitant with CTLA4-dependent signaling, this enabled the adoption of an incipient IL7R T cell phenotype. This study demonstrates that insulin binds together metabolic activity and histone acetylation in CD4 cells. Sufficient insulin signaling promotes IL7R memory phenotype accrual in aggressive PD1Tph cells. Hence, achieving insulin sensitivity via histone acetylation disarms effector CD4 T cell function and presents an attractive interventional goal to restore immune cell homeostasis in RA. - Source: PubMed
Publication date: 2026/05/25
Chandrasekaran VenkataragavanErlandsson Malin CSvensson DavidMalmhäll-Bah EricSilfverswärd Sofia TöyräPullerits RilleKatona GergelyBokarewa Maria I - Early fracture repairs are characterized by dynamic immune-skeletal interactions. While immune cells are known to be critical, how macrophage polarization (M1 to M2) and metabolism jointly shape the microenvironment repairs remains unclear. Here, we integrated three mouse long bone fracture sc/snRNA-seq datasets with multi-algorithm consensus annotation. Fracture expanded and rewired intercellular communication, with redistribution of incoming signaling toward immune populations, especially macrophage subsets, and increased relative flow through TGF-β, BMP, and FN1 pathways. From days 1 to 7 post-injury, macrophages followed a graded M1-to-M2 continuum, while M1-like cells remained prevalent across this interval. Distinct transcriptional programs were associated with M1-like and M2-like macrophages, with Creb3l2/Fos enriched in M1-like cells and Maf/Mafb enriched in M2-like cells alongside differential metabolic features. Data-driven prioritization across integrated public mouse omics datasets nominated Pbx3, Creb3l2, Nfix, Maf, and Mafb as candidate regulators associated with macrophage polarization, with spatial enrichment in macrophage-associated niches. A fracture-associated repair module comprised skeletal stem/progenitor cells (SSPCs), fibroblasts, macrophages, and osteoclasts, and was accompanied by predicted metabolite-mediated communication, with communication involving glutamine, sterol/cholesterol, and GABA prioritized as relatively increased and communication involving heme and 27-hydroxycholesterol as relatively reduced. SSPC lineage tracing revealed Taco1 as an early dynamic marker and branch-specific drivers, Runx2/Egfr (osteogenesis), Ebf1 (chondrogenesis), and Stat5a (adipogenesis). Collectively, these findings provide a computational atlas of early fracture healing, suggest that macrophages may play an important coordinating role during this stage, and prioritize transcriptional and metabolic candidates for future experimental validation. - Source: PubMed
Publication date: 2026/05/15
Chen HangLei ChangYeo Giselle CLim Khoon SXu Chun