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
- - 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
Çelik BesneKiraz YağmurŞahin YarenTezcanlı Kaymaz Burçin - Selective inhibition of the transcription factor STAT5b is challenging owing to the high degree of similarity to the family member STAT5a. We recently reported catechol bisphosphates as selective inhibitors of STAT5b, with Stafib-2-CR as the most potent selective STAT5b inhibitor reported to date. Here, we describe the design and synthesis of fusion molecules between Stafib-2-CR and a ligand of the E3 ligase cereblon in an effort toward STAT5b-selective proteolysis-targeting chimeras (PROTACs). The fusion molecules retain their activity against STAT5b in competitive fluorescence polarization assays, and the most potent compound is equally active against STAT5b as Stafib-2-CR, indicating that the choice of exit vector and linker is suitable for binding to STAT5b. However, conversion of the most potent fusion molecule into a cell-permeable prodrug turned out to be difficult, pointing toward the challenges of combining prodrug strategies with PROTAC technology. - Source: PubMed
Münzel TheresaSeidenstücker Karl ChristianProtzel ChristophBerg AngelaBerg Thorsten - Pheromones are key modulators of reproductive behavior in fish, and certain odorant receptors (ORs) expressed in the olfactory epithelium act as receptors for sex pheromones. The northern snakehead (Channa argus) exhibits distinctive parental care behaviors, such as nest construction and brood guarding. It is likely that hormonal regulation during the breeding season upregulates the expression of olfactory receptors, thereby enhancing the sensitivity of C. argus to pheromones released by the opposite sex and ultimately promoting the initiation of reproductive behaviors. A total of 256 functional OR genes were identified from the C. argus genome, and these were distributed across four chromosomes. Transcriptome sequencing of whole-brain and olfactory rosette tissues from males during and after the breeding season showed a marked upregulation of the olfactory receptor gene caor67 in the olfactory rosettes, as well as increased expression of prolactin (PRL) in the brain. The open reading frames (ORFs) of caor67, prl, prlra, prlrb, stat5a, and stat5b from northern snakehead were cloned and characterized. The expression of caor67 is highest in the olfactory rosettes. During the breeding season, the expression of caor67 in the male olfactory rosettes is significantly higher than in females. prl expression is relatively high in the pituitary, while prlra shows the highest expression in the gills, followed by the olfactory rosettes. prlrb has the highest expression in the olfactory rosettes, followed by the gills and kidney. In situ hybridization results show that the mRNA of caor67, prlra, and prlrb is expressed in the sensory epithelium of the C. argus olfactory rosettes, with expression detected in both ciliated and microvillous olfactory receptor neurons (ORNs). Co-localization of caor67 with prlra and prlrb was observed in the ORNs of the olfactory rosettes. Recombinant C. argus PRL (rPRL) was expressed and purified, and functional assays confirmed that it interacts with both PRLRa and PRLRb to enhance phosphorylated STAT5 (pSTAT5) activity. Overexpression of PRLRa/PRLRb or STAT5a/STAT5b significantly increased caor67 promoter-driven luciferase activity in vitro. Treatment with the JAK2 inhibitor TG101348, which blocks the JAK2-STAT5 signaling pathway, significantly reduced luciferase activity, indicating that PRL regulates the transcription of caor67 via the PRLR-JAK2-STAT5 signaling pathway. - Source: PubMed
Publication date: 2026/04/13
Jiang TianyuZuo ChenpengLyu LikangWang XiaojieSun DongleiJing XiaoYang XinlinQi Xin - Natural killer (NK) cells are key effectors in antitumor immunity, yet their function is markedly suppressed by transforming growth factor-β (TGF-β) in the tumor microenvironment. SMAD7 is an established intracellular antagonist of TGF-β signaling, but its specific role within NK cells remains poorly defined. - Source: PubMed
Publication date: 2026/04/09
Li JinLiu TingtingXiao WenganZhao DanLi QianLiu ShunanLi XinTong YiLi HuiminJiang HuaWu ShuangjieLi ZonghaiTu HongGan Yu