Ask about this productRelated genes to: STAT5B antibody
- Gene:
- STAT5B NIH gene
- Name:
- signal transducer and activator of transcription 5B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-01-28
- Date modifiied:
- 2019-04-23
Related products to: STAT5B antibody
Related articles to: STAT5B antibody
- In flatfish aquaculture, labour-intensive tank cleaning represents a major operational challenge, limiting sustainability due to its high labour requirements and associated costs. We tested a new semi-closed recirculating aquaculture system (RAS) protocol for (tongue sole), replacing manual cleaning with post-feeding water exchange (80% drained) and probiotic application. Compared with control groups, the probiotic-water exchange protocol significantly improved growth (+0.18%/day) and survival (+7.9%), while shifting the gut microbiota from a -dominated configuration to a -dominated one. Metagenomics revealed that became the predominant taxon (86%) in the probiotic group, accompanied by the enrichment of quorum sensing pathways, CAZymes (CEs, AAs), and nutrient metabolism functions. Histological examination showed improvements in the intestinal muscular layer and villi structure. Multi-tissue transcriptomics identified systemic changes in immune and metabolic pathways, including activation of intestinal immune networks (IgA production, NF-κB signaling) and antimicrobial peptide genes. Liver, gill, and skin transcriptomes revealed enhanced DNA repair, cytokine signaling, and barrier pathways. JAK-STAT pathway was also activated, linking microbial metabolite sensing to growth promotion (). The probiotic-integrated protocol modifies the gut microbiome by shifting microbial composition through changes in competitive interactions and microbial signaling pathways. It also improves the intestinal wall, overall immunity, and nutrient absorption. These findings provide insights into the microbiome-host interaction under probiotic treatment and suggest that this strategy may offer potential benefits under farm conditions, but further studies are needed to validate its safety and ecological implications. - Source: PubMed
Publication date: 2026/04/23
Hu YuanriYan XuGao FengtaoXu DanYang YingmingCheng JiayuChen SonglinCui Zhongkai - Not available. - Source: PubMed
Publication date: 2026/05/07
Su ZhanFeng Xianqi - - Source: PubMed
Publication date: 2026/05/05
Turingan Mark AnthonyWei CuihongAlmokhtar NihadVijenthira AbiChang Hong - Growth hormone (GH) signaling through STAT5B is a central regulator of hepatic metabolism, yet the functional consequences of disease-associated STAT5B variants remain poorly understood. Here, we analyzed mice carrying STAT5BY665F (gain-of-function) and STAT5BY665H (loss-of-function) variants and dissect their impact on metabolic regulation. STAT5BY665F mice developed hypercholesterolemia and enhanced insulin sensitivity, whereas STAT5BY665H mice displayed reduced body weight and impaired insulin responsiveness. Transcriptomic analyses revealed that STAT5BY665F activated lipid, cholesterol, and immune transcriptional programs, while STAT5BY665H failed to induce these pathways. Notably, STAT5BY665F substantially feminized male liver gene expression, inducing 77% of female-biased genes while repressing 51% of male-biased genes, thereby mimicking the persistent STAT5B activation characteristic of female livers. ChIP-seq demonstrated extensive STAT5BY665F enhancer occupancy at metabolic and immune loci, contrasting with the minimal chromatin engagement of STAT5BY665H. Beyond the liver, STAT5BY665F broadly reprogrammed adipose tissue gene expression, activating lipid metabolism and immune regulatory networks, whereas STAT5BY665H exerted more restricted effects. Together, these findings illustrate how alterations in STAT5B activity affect enhancer activation and can lead to changes in metabolic function and hepatic sexual dimorphism. - Source: PubMed
Publication date: 2026/05/05
Lee Hye KyungPyatkov MaximGavrilova OksanaLiu NailiDemby TamarYe BingtianFurth Priscilla AHennighausen LotharWaxman David J - Breast carcinoma is a major cause of cancer-related mortality among women worldwide. Identifying novel molecular targets remains essential, particularly for aggressive triple-negative breast cancer (TNBC). Leucine-rich alpha-2-glycoprotein 1 (LRG1) has been linked to tumor progression and angiogenesis, but its molecular mechanisms in breast cancer are poorly defined. We evaluated the effects of recombinant human LRG1 (rhLRG1) on cell viability and migration in MDA-MB-231 TNBC cells and performed transcriptomic profiling followed by functional enrichment analyses using GenArise, Cytoscape, and R-based tools. RhLRG1 treatment significantly increased cell viability and migration. Transcriptomic analysis revealed activation of key oncogenic cascades, including the PI3K/AKT, MAPK, and RAS signaling pathways. Hub-gene analysis identified upregulated genes involved in proliferation (, , ), angiogenesis (, ), and apoptosis (, ), whereas downregulated genes were associated with apoptotic resistance (, ) and adhesion (, ). Functional enrichment highlighted LRG1's role in the bioinformatic analysis of differentially expressed genes that were obtained from microarray assays. LRG1 remodels the tumor microenvironment by promoting proliferation, angiogenesis, and apoptotic sensitivity while repressing resistance-related genes. These findings position LRG1 as a potential diagnostic biomarker and therapeutic target for advanced breast carcinoma. - Source: PubMed
Publication date: 2026/04/18
Osorio-Antonio FedericoDiaz-González Daniela MichelCampos-Viguri Gabriela ElizabethSánchez-López José ManuelCortez-Sánchez José LuisCastelán FranciscoChávez-Rios Jesús RamsesMaycotte-González PaolaCortés-Hernández PaulinaPeralta-Zaragoza OscarBautista-Rodríguez Elizabeth