STAT5A Antibody (Ab-694), pAb, Rabbit
- Known as:
- STAT5A Antibody (Antibody-694), pAb, Rabbit
- Catalog number:
- A00280-100
- Product Quantity:
- 100,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- STAT5A Antibody (Ab-694) pAb Rabbit
Related genes to: STAT5A Antibody (Ab-694), pAb, Rabbit
- 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 (Ab-694), pAb, Rabbit
Related articles to: STAT5A Antibody (Ab-694), pAb, Rabbit
- 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 - Cardiac fibrosis, a maladaptive remodeling process following myocardial infarction (MI), is a key driver of heart failure, the precise molecular regulators governing cardiac fibroblast activation remain incompletely understood. LIM and cysteine-rich domains 1 (LMCD1) has been shown to promote renal and lung fibrosis, but its role in cardiac fibrosis is unknown. We hypothesized that LMCD1 promoted cardiac fibrosis post-MI. Re-analysis of publicly available single-cell RNA sequencing datasets revealed a significant upregulation of LMCD1 in cardiac fibroblasts after MI. LMCD1 was upregulated in mouse hearts subjected to left anterior descending (LAD) artery ligation and in primary cardiac fibroblasts stimulated with TGF-β1. Silencing of LMCD1 improved cardiac function (increased ejection fraction and fractional shortening) and reduced fibrotic area, concomitant with decreased fibrosis-related proteins (fibronectin, COL1A1, and α-SMA). In TGF-β1-induced primary cardiac fibroblasts, LMCD1 knockdown inhibited cell proliferation and fibrosis-related proteins expression, while its overexpression showed the opposite trend. Mechanistically, pathway enrichment analysis linked LMCD1 to the IL2-STAT5 signaling. LMCD1 silencing reduced the phosphorylation and total protein levels of STAT5A in infarcted mouse heart tissues. Co-immunoprecipitation assays confirmed a direct interaction between LMCD1 and STAT5A. Furthermore, STAT5A overexpression reversed the inhibitory effect of LMCD1 knockdown on TGF-β1-induced fibrosis in primary cardiac fibroblasts. In conclusion, our study identifies LMCD1 as a novel driver of post-MI fibrosis, which functions by activating STAT5A in cardiac fibroblasts, offering a potential new target for anti-fibrotic therapy. - Source: PubMed
Publication date: 2026/04/30
Kang HaofeiLiu JingWang JunjieZhang Yunrui - Feed behavior traits are directly linked to the sustainability of pig production. This study aimed to investigate the genetic basis of feeding behavior traits in Landrace and Yorkshire pigs, focusing on genomic regions, quantitative trait loci (QTL), candidate genes, and metabolic pathways associated with these traits. - Source: PubMed
Publication date: 2026/04/10
Gervásio Izally CarvalhoBrito Luiz FAraujo Andre CFanalli Simara LarissaSilva-Vignato BárbaraRocha Artur OBenfica Lorena FerreiraFernanda de Oliveira LeticiaFelício Ament Andrezza MariaMonteiro Moreira Gabriel CostaMoncau-Gadbem Cristina TschornyMello Cesar Aline Silva - - Source: PubMed
Publication date: 2026/04/25
Salmani MahyarRastegari-Pouyani MohsenAfshar SaeidTalebi-Ghane ElahehEftekharian Mohammad Mahdi