STAT5A Antibody (Ab-694), pAb, Rabbit
- Known as:
- STAT5A Antibody (Antibody-694), pAb, Rabbit
- Catalog number:
- A00280-100
- Product Quantity:
- 100,0μg
- 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
- The clinical use of glucocorticoids often leads to skeletal muscle injury, characterized by muscle atrophy and dysfunction. Fibro-adipogenic progenitors (FAPs) play an important role in maintaining muscle homeostasis, but their roles in the recovery of skeletal muscle after glucocorticoid-induced injury remain largely elusive. Here, we reveal that glucocorticoid induces cellular senescence of FAPs, leading to their accumulation in skeletal muscle. Mechanistically, glucocorticoid enhances the expression of GFPT2 through STAT5A, which further elevates O-GlcNAcylation in FAPs and promotes their senescence. Targeting the STAT5A-GFPT2-mediated O-GlcNAcylation can reduce the burden of senescent FAPs in glucocorticoid-treated muscle and facilitate muscle recovery after injury. Our results demonstrate that exosomes derived from senescent FAPs suppress myotube formation, greatly inhibiting the regrowth of glucocorticoid-treated skeletal muscle. Moreover, senescent FAPs reduce the muscle stem cells (MuSCs) pool by suppressing their proliferation, thereby impairing the regenerative capacity of skeletal muscle during the recovery process after glucocorticoid treatment. - Source: PubMed
Publication date: 2026/09/16
Li BingfeiXiang WeiQi WanwanLiu XinxinZhu WeiwenZhang WeiJin RunzeMa ShuoChen LifengBai ChuanqingFang ShunzhengWu JiangyiZhang XiaoqiDai LimengGuan XingyingLi JiaLi SongXiong YanFang XiangqinGao ChangyueZhou SiruGuo HongNi Zhenhong - This study investigated the molecular characteristics and functions of buffalo prolactin (PRL) in the lactation. The buffalo gene's complete coding sequence (CDS) is 690 bp, encoding 229 amino acids, with structure and function highly consistent with other Bovidae species. expression was significantly higher in the buffalo mammary gland during lactation compared to the non-lactating period, highlighting its crucial role in lactation. overexpression in buffalo mammary epithelial cells (BuMECs) promotes cell proliferation and increases the casein secretion and triglyceride (TAG) accumulation. This occurs through the activation of the JAK2-STAT5 (cell differentiation, casein () gene transcription, and lipid factor transcription), PI3K-AKT-mTOR (cell growth, milk protein gene translation, and lipid factor activation), and mitogen-activated protein kinase (MAPK; cell proliferation and stress mitigation) signaling pathways. Specifically, overexpression upregulated the mRNA expression of genes in these pathways, such as , , , , , , and , while decreasing and . Overexpression also increased the expression of cell cycle genes (, , /), and enhanced cell viability. Furthermore, overexpression led to increased expression of casein genes (, ) and milk-fat-synthesis-related genes (, , , , ). Population genetic analysis identified five single-nucleotide polymorphisms (SNPs) in the buffalo CDS, with c.34C T and c.430T C being non-synonymous substitutions that were predicted to affect protein function. This research provides a theoretical foundation for genetic interventions aimed at improving buffalo lactation traits. - Source: PubMed
Publication date: 2025/12/03
Huang LigeFan XinyangTeng XiaohongQian LindongBao ZhipengMiao Yongwang - As the global population continues to grow, the demand for protein is correspondingly increasing. Milk serves as a significant source of high-quality protein, with casein being its primary nutrient. Consequently, the cultivation of dairy animals with elevated casein expression has become a critical objective in the field of livestock breeding. Compared with traditional breeding methods, gene editing offers a more efficient approach to enhancing casein expression in dairy animals. However, progress in this area is constrained by the lack of key editing targets. Enhancers, which are core cis-acting elements enriched with transcription factor and cofactor binding sites, play a crucial role in regulating milk protein expression and represent ideal targets for gene editing. At present, comprehensive research on enhancers at the casein gene locus in livestock remains limited. This study identified 8 ultra-conserved regions through a cross-species comparison of casein gene loci in humans, mice, cattles, zebu cattle, goats, sheep, and camels. Following functional validation in silico, cross-species conserved enhancer sequences regulated by STAT5a were validated, with the CSN2 conserved enhancer (CSN-EN3) demonstrating the most potent regulatory effect. Co-immunoprecipitation (Co-IP) and bimolecular fluorescence complementation assays have demonstrated that STAT5a interacts with cofactors such as MED1, GR, ELF5, and NFIB, thereby synergistically regulating gene expression. The findings suggest that transcription factors and cis-acting elements associated with lactation exhibit high interspecies conservation, elucidating the pivotal role of STAT5a in lactation regulation. By altering the conserved enhancer CSN-EN3, its cis-regulatory control over STAT5a-dependent transcription was changed, leading to a 3.57-fold increase in casein expression. In conclusion, this study developed an enhancer identification system that integrates multi-species genome alignment with model animal epigenetic marker analysis, successfully identifying cross-species conserved enhancers at the mammalian casein locus. This research introduces a novel strategy to augment casein expression in ruminants, providing a significant theoretical foundation and technical support for the precision breeding of high-casein dairy cows and goats. - Source: PubMed
Publication date: 2026/08/25
Zhu ZhenliangMi XiaoyuYu WeiLiu YayiZhang YongJian YangyiMa XiaodanZhou QunliTang JiaomeiFeng RuiGao YuanpengLiu Jun - Recently, we have shown that exposure to the ultraviolet filter benzophenone-3 (BP3) during secretory differentiation disrupts prolactin signaling pathway and milk protein expression in murine mammary organoids. The present study aimed to evaluate whether intrauterine exposure to BP3 modifies the functional differentiation of the lactating mammary gland in F1 female mice. To this end, pregnant mice (F0) were dermally exposed to BP3 (0.15 or 50 mg/kg/day) or the control vehicle (sesame oil), from gestation days 8.5-18.5. After delivery, F0 dams nursed their pups, and F1 female offspring were subsequently bred at 8 weeks of age. Lactation day (LD) 1 was defined as the day following the birth of F2 litters and lactating mammary glands of F1 females were examined on LD10. BP3 exposure did not affect the body weight of the F1 females or that of their F2 litters. Intrauterine exposure to BP3 significantly altered alveolar size and myoepithelial cell density at mid-lactation. However, the expression of milk proteins and the mRNA levels of Stat5a and Elf5 were similar to those of control animals. These findings reveal a subclinical mammary phenotype in which intrauterine BP3 exposure alters alveolar organization and the myoepithelial compartment while preserving lactational output, consistent with a reduction in mammary functional reserve without overt impairment of milk production or offspring growth. - Source: PubMed
Publication date: 2026/08/20
Schierano-Marotti GonzaloAltamirano Gabriela AGomez Ayelen LOddi SofiaRodríguez Horacio AKass Laura - Chemotherapy-induced peripheral neuropathy (CIPN) lacks disease-modifying therapies, and how epitranscriptomic regulation drives central sensitization remains unclear. In the present study focusing on paclitaxel-induced peripheral neuropathy (PIPN), we identified a METTL3-circRNA axis in the spinal dorsal horn wherein upregulated METTL3 expanded the m6A-modified circMtmr7 pool in paclitaxel-treated mice. Accordingly in paclitaxel-treated mice, upregulated METTL3 paralleled elevated m6A-circMtmr7 expression; METTL3 knockdown prevented the paclitaxel-evoked rise in m6A-circMtmr7, normalized miniature excitatory postsynaptic current (EPSC) amplitude and frequency, as well as neuronal firing rates, and alleviated mechanical allodynia. Mechanistically circMtmr7 operated via two convergent branches to upregulate the effector NUFIP2: (i) in the cytoplasm it served as a microRNA (miRNA) sponge for miR-7010-5p, miR-3057-5p and miR-26b-3p, relieving repression and increasing NUFIP2; (ii) in the nucleus it associated with STAT5A to enhance NUFIP2 transcription, and silencing STAT5A reversed neuronal hyperexcitability and attenuated nociceptive behaviours. Genetic or pharmacological manipulation of METTL3, circMtmr7, STAT5A or NUFIP2 bidirectionally modulated neuronal excitability and nociceptive hypersensitivity. Collectively these data establish an m6A-dependent writer-circRNA-transcription factor hub that couples post-transcriptional and transcriptional programmes to amplify excitatory drive in PIPN, suggesting that STAT5A and NUFIP2 represent candidate targets for therapeutic development. KEY POINTS: In paclitaxel-treated mice, spinal dorsal horn METTL3 is upregulated, expanding the m6A-modified circMtmr7 pool to drive central sensitization in paclitaxel-induced peripheral neuropathy. circMtmr7 convergently upregulates NUFIP2 by acting as a cytoplasmic microRNA (miRNA) sponge and by associating with nuclear STAT5A to enhance transcription, thereby amplifying neuronal excitability. Pharmacological or genetic inhibition of METTL3, circMtmr7, STAT5A or NUFIP2 alleviates paclitaxel-induced nociceptive hypersensitivity. - Source: PubMed
Publication date: 2026/08/20
Ou ChaopengHe ZhaoliWang SudenaHuang JingxiuLi NaChi DongmeiZhang KunGuo JinOuyang HandongBai Xiaohui