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
- 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 - ATL is an aggressive T-cell malignancy with a poor prognosis that is caused by HTLV-1 infection. We previously demonstrated that NDRG2 is significantly downregulated in ATL, resulting in aberrant activation of the signal transduction pathways through the dissociation of serine/threonine phosphatase PP2A. To identify potential targets of NDRG2, we performed comprehensive mass spectrometry of differentially phosphorylated peptides in ATL cells with overexpression of NDRG2 using a TiO-based enrichment method. KEGG and GO analysis revealed that the downregulated phosphopeptides correlated with signaling pathways, T-cell differentiation, and proliferation. Our results identified STAT5B as a novel NDRG2-regulated protein that is dephosphorylated at serine 193 and tyrosine 699. Although enforced expression of NDRG2 in ATL cell lines does not change the phosphorylation of JAK3, an upstream regulator of STAT5, phosphorylated STAT5 at tyrosine and serine is significantly suppressed by the direct binding to STAT5 with NDRG2 leading to the inhibition of STAT5 downstream gene expression. Furthermore, NDRG2 binds to STAT5B with alanine replacement of Y699 (Y699A) but only weakly is associated with S193A, suggesting that NDRG2 is directly involved in serine phosphorylation through the recruitment of PP2A to STAT5. Because S193A remarkably induces reduced phosphorylation of Y699 and subsequent transcriptional activity, the induction of serine phosphorylation through the loss of NDRG2 expression is dispensable for STAT5 tyrosine phosphorylation and activity. Since the loss of NDRG2 expression is essential factor to maintenance of ATL cells by STAT5 activity through phosphorylation of serine and tyrosine, targeting STAT5 becomes a feasible and effective strategy in NDRG2-deficient ATL. - Source: PubMed
Publication date: 2026/04/27
Ichikawa TomonagaNakahata ShingoShimoda KazuyaMurakami TakashiMorishita Kazuhiro - Sorghum is known for its anti-cancer, anti-inflammatory, and antioxidant properties, but its effect on cell growth is not well understood. First, the cytotoxicity of various sorghum extract (SE) concentrations was evaluated in C2C12 (murine myoblasts) and C3H10T1/2 (murine embryonic fibroblasts). The extent of DNA damage was then assessed, and the activation of the JAK2/STAT5b and IGF-1 pathways was observed. Studies on the transcriptional regulatory function of STAT5b revealed that SE increased STAT5b/DNA binding and transcriptional promoter activity. Consequently, STAT5b upregulation led to the increased expression of IGF-1. Moreover, other factors, such as growth hormone receptor and bone morphogenetic protein 7, were also upregulated. The results of these experiments suggest that sorghum may enhance muscle recovery or promote growth factors by stimulating the JAK2/STAT5b and IGF-1 pathways. Therefore, sorghum is expected to be an effective functional food for bone growth and muscle recovery, without inducing adverse side effects. - Source: PubMed
Publication date: 2026/04/09
Park SanghyeonKang Dong YoungKim Hyo TaeShin Woo-ShikLee SangwonCho JaehoonJang Kyoung-Jin - Feed behavior traits are directly linked to the sustainability of pig production. This study aimed to investigate the genetic basis of feeding behavior traits in Landrace and Yorkshire pigs, focusing on genomic regions, quantitative trait loci (QTL), candidate genes, and metabolic pathways associated with these traits. - Source: PubMed
Publication date: 2026/04/10
Gervásio Izally CarvalhoBrito Luiz FAraujo Andre CFanalli Simara LarissaSilva-Vignato BárbaraRocha Artur OBenfica Lorena FerreiraFernanda de Oliveira LeticiaFelício Ament Andrezza MariaMonteiro Moreira Gabriel CostaMoncau-Gadbem Cristina TschornyMello Cesar Aline Silva