STAT5A Antibody (Ab_694), pAb, Rabbit
- Known as:
- STAT5A Antibody (Ab_694), pAb, Rabbit
- Catalog number:
- A00280
- Product Quantity:
- 40ug
- 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
- Signal transducer and activator of transcription 5 A (STAT5A) modulates breast cancer cell proliferation and metastasis, yet its epigenetic regulatory mechanisms and impacts on the tumor immune microenvironment (TIME) remain unclear. Here, we explored STAT5A's epigenetic traits, metastatic roles, and effects on tumor-associated immune cells via two mouse models (immunodeficient vs. immunocompetent) with metastasis established by tail vein injection or orthotopic tumorigenesis, flow cytometry to characterize immune cell subsets, cell co-cultures, clinical tissue analyses, and dCas9-TET1CD-mediated STAT5A promoter methylation intervention. Low STAT5A expression reduced tumor cell proliferation but enhanced migration/invasion, with in vivo metastatic capacity dependent on TIME. Tumors with low STAT5A expression grew slower and metastasized less in immunodeficient mice, but exhibited opposite phenotypes in immunocompetent cohorts. Mechanistically, STAT5A downregulation was associated with epithelial-mesenchymal transition (EMT), cytokine pathway remodeling, impaired T-cell cytotoxicity, and macrophage-associated immunosuppressive remodeling. Macrophage-derived LIF activated STAT5A phosphorylation via LIFR. Clinical samples showed sequentially increasing STAT5A promoter methylation and decreasing protein expression from normal tissues to primary/metastatic tumors. dCas9-TET1CD-mediated targeted demethylation restored STAT5A expression and reduced cell migration. These findings suggest that epigenetic silencing of STAT5A contributes to breast cancer metastasis through coordinated regulation of EMT-like plasticity and the TIME, and support further investigation of STAT5A reactivation or LIF-LIFR modulation as potential anti-metastatic strategies. - Source: PubMed
Publication date: 2026/06/29
Yang XueSu YuhangYing YushiPeng YouyunWang RuyuanXu ShaojieZhao YuxiShu XinPeng QiyueLi XingruiDu Yaying - Prolactinomas are typically benign but represent a major cause of endocrine dysfunction. However, their molecular subtypes remain undefined, and clinical implications of such subtypes are unclear. The objective of this study was to characterize the genomic subtypes of prolactinomas and evaluate associated clinicopathological and immunological features. - Source: PubMed
Publication date: 2026/06/26
Wang Da PengLiu Yan TingDai Yu TingChen De ShengCheng Yi JunLin Shao JianZhang YanXue LiXie JingWu Zhe Bao - As important post-transcriptional and epigenetic regulators of gene expression, miRNAs play a pivotal role in modulating host-virus interactions. While prior reviews have addressed either direct miRNA-HIV genome interactions or miRNA-mediated immune modulation in isolation, the integrated dual functionality of these molecules has not been systematically characterized. This review aimed to comprehensively explore how miRNAs that target the HIV-1 genome simultaneously modulate key innate and adaptive host immune signaling pathways. The conceptual novelty of this study is determined not by the identification of previously unknown miRNA-target gene pairs, but by the systemic integration of two regulatory levels (direct inhibition of the viral genome and modulation of the host cell immune signaling pathways) within a unified analytical framework. Such an integrated approach reveals a proviral regulatory network that remains non-obvious when each of these levels is examined separately. - Source: PubMed
Publication date: 2026/06/05
Timofeeva Anna MAulova Kseniya SNevinsky Georgy A - Triple-negative breast cancer (TNBC) remains lethal due to paucity of targetable markers. MicroRNAs are involved in TNBC pathogenesis; however, their clinical translation in TNBC remain limited. We evaluated miR-6809 and miR-4753 expression in TNBC tissues, their potential as diagnostic biomarkers, and their correlations with tumor-related data. - Source: PubMed
Publication date: 2026/06/19
Taha MohamedMekhael EmadAbd-Al Aziz Ahmed - Abnormal accumulation of Poly(ADP-ribose) polymerase 1 (PARP1) promotes cancer progression, yet its stabilization mechanisms remain unclear. Here, we identify E3 ubiquitin ligase tripartite motif-containing 21 (TRIM21) as a PARP1-binding partner. PARP1 interacts directly with TRIM21 via its 662-908 domain, while the PRY-SPRY domain of TRIM21 is essential for this binding. TRIM21 facilitates PARP1 polyubiquitination at residue K654, leading to its degradation. In small cell lung cancer (SCLC), TRIM21 is significantly downregulated, and its tumor-suppressive function is partly mediated through the degradation of PARP1, supporting genomic stability. Additionally, the PI3K/AKT pathway transcriptionally suppresses TRIM21 via transcription factor STAT5A, thereby stabilizing PARP1. Importantly, combining the PI3K/AKT inhibitor PKI-587 with the PARP inhibitor BMN673 synergistically inhibits tumor growth across multiple SCLC models, including cell lines, patient-derived organoids, and xenograft models. Collectively, our findings define a "PI3K/AKT-STAT5A-TRIM21-PARP1" axis critical for SCLC progression and propose its dual inhibition as a promising therapeutic strategy. - Source: PubMed
Publication date: 2026/06/18
Cao GuozhenLi GongfengWang XiaolinZhang TengfeiYao XinhuangHou PengZhang JiahuiGuo XiaopengWang JiarongXiang LiJi HongbinGuo ChenchenLin Wenchu