STAT5A (Phospho_Tyr694) Antibody
- Known as:
- STAT5A (Phospho_Tyr694) Antibody
- Catalog number:
- E011048-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- STAT5A (Phospho_Tyr694) Antibody
Ask about this productRelated 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
- 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 - Plasma cell myeloma is a heterogeneous hematologic malignancy characterized by clonal expansion of plasma cells. While RAS-MAPK pathway mutations are known high-risk features, the clinical relevance of STAT3/STAT5 mutations remains unclear. - Source: PubMed
Publication date: 2026/04/08
Ye Matthew TZuo ZhuangCalin StelianaYang YalingYou M James - Fostering STAT5 signaling is key to immunotherapies that leverage CD8 T cell biology. Using mouse models, we demonstrate that the two mammalian STAT5 paralogs, STAT5A and STAT5B, are at once redundant and functionally distinct in CD8 T cells. Thus, they are asymmetric paralogs, exhibiting both widespread homology at molecular level and functional asymmetry at cellular level, with STAT5B emerging as dominant. For mechanisms, we determined that STAT5B is twice as abundant, accounting for two-thirds of the total STAT5 pool, and present evidence that it also has distinct, paralog-specific properties. We also defined cytokine- and cell state-restricted STAT5B functions and devised a core signature that spotlights key downstream properties and serves as bioinformatic probe. Together, these studies affirm the centrality of STAT5 in CD8 T cells, reveal common and circumscribed activities for STAT5A and STAT5B, and present a unifying model that foregrounds both redundancy and asymmetry. - Source: PubMed
Publication date: 2026/04/04
Ristin SvetlanaDalzell MollyArmstrong ChristopherIlsin NisaFontanella Antonio MNivelo LuisHennighausen LotharO'Shea John JVillarino Alejandro V