STAT5A (Phospho_Ser780) Antibody
- Known as:
- STAT5A (Phospho_Ser780) Antibody
- Catalog number:
- E011049-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- STAT5A (Phospho_Ser780) Antibody
Related genes to: STAT5A (Phospho_Ser780) 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_Ser780) Antibody
Related articles to: STAT5A (Phospho_Ser780) Antibody
- Fetal growth restriction (FGR) is a complex condition with highly heterogeneous clinical outcomes, making prenatal distinction between transient and persistent growth failure challenging. This study aims to identify amniotic fluid (AF) biomarkers capable of differentiating distinct FGR trajectories and characterizing persistent growth failure mechanisms. - Source: PubMed
Publication date: 2026/08/15
Cao YanHao WenjingWang YanChai ChongchongLi YouranLiu YingZhu HongyuanLu YifanWang DongZhai YanhongYan YoushengCao Zheng - STAT5A is unique in its diverse expression in different cells. Here, we show that STAT5A deficiency results in reduced expression of the actin-bundling protein α-actinin-1, which alters cytoskeletal reorganization, including loss of actin bundles, reduction of cellular motility, and clustering of mitochondria and endoplasmic reticulum in the perinuclear region. These changes in cellular architecture led to production of ROS by the mitochondria, which may be explained by reduced peroxisome abundance. This, in turn, results in dsDNA breaks and formation of cytoplasmic micronuclei, and activating the cGAS-STING pathway, and mediating type I IFN production and the expression of IFN-stimulated genes. The ectopic expression of α-actinin-1 or STAT5A in STAT5A knockout cells is sufficient to restore actin bundle formation and nullifies all downstream effects. Conversely, inhibiting downstream steps suppresses only subsequent events in the pathway. STAT5A knockout results in a similar phenotype as seen with cytochalasin B, an inhibitor of actin polymerization. Overall, we show that STAT5A-α-actinin-1 links cytoskeleton integrity to mitochondrial immune regulation. - Source: PubMed
Publication date: 2026/08/07
Sun BoyueKrishnamohan MathumathiNevo ReinatZoler EyalElbaz-Alon YaelGeiger BenjaminSchreiber Gideon - Breast Cancer (BCa) remains the leading cause of cancer-related mortality among women, underscoring the need for developing more effective novel biomarkers. This study investigated the role of Growth Arrest-Specific 2 (GAS2) and its co-expressed genes in breast cancer. - Source: PubMed
Publication date: 2025/11/03
Rahimi SaminHaghi MehdiNajarzadeh DariushHosseinpour Feizi Mohammad Ali - Solute carrier (SLC) family genes govern transmembrane transport and cellular metabolism, yet their systematic roles from Helicobacter pylori infection to gastric cancer (GC) remain undefined. By integrating multiple GEO datasets with weighted gene co-expression network analysis, differential expression, and machine learning algorithms, we identified seven core SLC genes (SLC9A9, SLC43A2, SLC16A6, SLC7A14, SLC28A3, SLC4A11, SLC5A2) for H. pylori infection and nine (SLC1A3, SLC2A3, SLC15A3, SLC19A3, SLC2A12, SLC16A4, SLC25A4, SLC9A7, SLC28A3) for GC. Logistic regression models achieved high diagnostic accuracy (AUC = 0.976 and 0.874, respectively). Immune infiltration analysis revealed distinct correlation patterns: SLC4A11 and SLC5A2 associated with activated mast cells, neutrophils, and M2 macrophages in infection, while SLC1A3 and SLC2A3 correlated broadly with M1/M2 macrophages and activated CD4 T cells in GC. Enrichment analyses confirmed involvement in transmembrane transport, immune-related pathways, and cancer signaling. Transcription factor prediction identified CEBPB, RELB, and STAT5A as key upstream regulators. Molecular docking demonstrated strong binding affinities between SLC proteins and repurposable compounds (3'-azido-3'-deoxythymidine, CHEMBL1182312, quinine). This study provides the first systematic characterization of SLC family expression across the H. pylori-GC continuum, identifying potential diagnostic biomarkers and therapeutic targets that warrant further experimental validation. - Source: PubMed
Publication date: 2026/07/25
Lv NuonanHe XueCai TingXu YingtingXie JieZhao XuelinYang BinfangLiu XuemeiZhang Minglin - Buffalo milk is favoured by consumers due to its higher nutritional components, as well as its rich and mellow flavour. However, research on the molecular mechanisms underlying the formation of lactation traits in buffalo remains limited. In this study, we systematically investigated the regulatory effects of estrogen receptor alpha () on lactation-related functions in buffalo mammary epithelial cells (BMECs) using overexpression and small interfering RNA (siRNA)-mediated silencing strategies. Our results demonstrated that knockdown via siRNA significantly suppressed BMEC viability and proliferation and downregulated the expression of genes associated with lipid transport and secretion (), milk protein synthesis (), and cell proliferation (). Concurrently, silencing markedly upregulated pro-apoptotic genes (, ) and downregulated the anti-apoptotic gene . Conversely, overexpression exerted opposite effects on BMECs, further validating the critical role of in modulating BMEC proliferation and milk component synthesis. In conclusion, expression enhances buffalo lactation traits by promoting milk fat and milk protein synthesis, stimulating BMEC proliferation, and inhibiting cellular apoptosis. These findings provide novel insights into the molecular mechanisms governing buffalo lactation and offer valuable references for the development and utilization of lactation-related genetic resources in buffalo breeding. - Source: PubMed
Publication date: 2026/06/25
Wang ZhixiangChen XiaoyunQin ChaobinJiang JiaqiLi LingLiu QingyouTeng CuijinXiong JinpingWang LeyiAmin AhmedLi Zhipeng