STAT5A (phospho-Tyr694) Antibody
- Known as:
- STAT5A (phosphorilated-Tyr694) Antibody
- Catalog number:
- abx000190
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- STAT5A (phospho-Tyr694) Antibody
Related genes to: STAT5A (phospho-Tyr694) 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 (phospho-Tyr694) Antibody
Related articles to: STAT5A (phospho-Tyr694) Antibody
- 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 - Therapeutic resistance to tyrosine kinase inhibitors (TKIs) remains a major challenge in the clinical management of chronic myeloid leukemia (CML). The transcription factor STAT5A, a principal downstream effector of BCR::ABL1, has emerged as a key transcriptional regulator implicated in the development of TKI resistance. This study aims to functionally validate the role of STAT5A in TKI-resistant CML by employing CRISPR/Cas9-mediated gene knockout and assessing the downstream molecular and phenotypic alterations. We hypothesized that selective disruption of STAT5A would restore apoptotic sensitivity and TKI responsiveness in resistant CML models. Additionally, we sought to integrate bioinformatic transcriptional network analyses to confirm whether STAT5A directly regulates the genes modulated by its deletion, thus reinforcing its mechanistic relevance as a therapeutic target. STAT5A was knocked out using CRISPR/Cas9 in K562 cells and their TKI-resistant derivatives (K562/Ima-Res, K562/Pon-Res). Western blot analysis confirmed effective depletion of STAT5A protein following CRISPR/Cas9 editing, validating that the observed phenotypic and transcriptional changes were attributable to successful STAT5A knockout. Post-editing, XTT assays were performed to assess cell viability, followed by Annexin V/PI staining for apoptosis and PI-based flow cytometry for cell cycle analysis. RT-qPCR was used to quantify the expression of key genes involved in the JAK/STAT pathway (JAK2, STAT3, CISH) and apoptosis/DNA damage responses (TP53, ATM, CASP3, CASP8). In silico analyses were conducted using TRRUST and Harmonizome/ChEA3 to confirm whether the genes modulated by STAT5A deletion were direct transcriptional targets. For additional validation, expression matrices from GSE207627 and GSE208314 were reanalyzed to confirm STAT5A-centered pathway alterations in resistant CML datasets. STAT5A knockout significantly reduced cell viability and induced apoptosis across all CML cell models, accompanied by G0/G1 cell cycle arrest. RT-qPCR revealed altered expression of both JAK/STAT components (JAK2, STAT3, CISH) and apoptosis-related genes (TP53, ATM, CASP3, CASP8). Transcriptional target analysis confirmed that several of these genes-such as CDKN2B, BCL2L1, and CCND1-are direct STAT5A targets, reinforcing the functional consequences of STAT5A loss. Integration of these findings suggests that STAT5A knockout reprograms both intrinsic (CASP3, TP53, ATM) and extrinsic (CASP8, BCL2L1) apoptotic pathways, thereby restoring chemosensitivity. CISH dysregulation further suggested compensatory feedback within the signaling network. CRISPR/Cas9-mediated STAT5A disruption effectively reverses TKI resistance in CML cells by reprogramming apoptotic and proliferative signaling. These findings identify STAT5A as a mechanistically validated and clinically actionable target, supporting its potential for combination strategies with TKIs or STAT5 inhibitors such as pimozide. Integration of transcriptional network analysis supports the mechanistic basis of these effects. STAT5A emerges as a compelling therapeutic target, meriting further investigation in preclinical models and patient-derived samples to evaluate its translational potential. Future validation in patient-derived CD34⁺ CML models may advance STAT5A-based therapeutic design. - Source: PubMed
Publication date: 2026/04/25
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