STAT5B & GHR Protein Protein Interaction Antibody Pair
- Known as:
- STAT5B & GHR Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0215
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- STAT5B & GHR Protein Interaction Antibody Pair
Related genes to: STAT5B & GHR Protein Protein Interaction Antibody Pair
- 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 & GHR Protein Protein Interaction Antibody Pair
Related articles to: STAT5B & GHR Protein Protein Interaction Antibody Pair
- 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 - To investigate selected transcripts from urinary cells regarding their potential to predict risk reclassification in patients with prostate cancer (PCa) on active surveillance (AS). - Source: PubMed
Publication date: 2026/08/20
Borkowetz AngelikaGräfe SebastianKwe JeremyFuessel SusanneThomas ChristianErdmann Kati - : Identifying molecular liabilities and understanding disease heterogeneity are prerequisites for advancing therapies in T-cell prolymphocytic leukemia (T-PLL), a rare T-cell malignancy with a poor prognosis. : RNA-seq profiling of T-PLL samples ( = 10) and the normal counterpart ( = 5) allowed us to report gene expression and pathway alterations in malignant cells, revealing that non-coding, antisense and circular RNA expression is profoundly altered in T-PLL. : T-PLL displayed activation of several oncogenic pathways, particularly PI3K/AKT/mTOR and Wnt, suppression of healthy T-cell activities and cell death escape. Tumor suppressor lncRNAs (, and ) with reduced expression and upregulated oncogenic pro-proliferative lncRNAs (, , and ) were identified. CircRNAs ectopically expressed in T-PLL included circSEMA4B and circSATB1, linked to the Wnt pathway, circFIRRE and oncogenic circPVT1 and circFKBP5. Focusing on five genes with validated recurrent oncogenic variants (, , , , and ), we investigated genotype/phenotype relations. A multiple predictor linear model suggested potential links between driver variants and alterations in gene and circRNA expression, including association between mutations and upregulation, lesions and increased expression along with suppression. : Our transcriptomic profiling and genotype-phenotype association analysis identified specific genes, non-coding RNAs, pathways and candidate genotype-associated transcriptional signatures that warrant further investigation as potential targets for the development of new therapeutic approaches for this rare and heterogeneous malignancy. - Source: PubMed
Publication date: 2026/07/29
Gasparini Vanessa RebeccaOrsi SilviaBuratin AlessiaRampazzo ElisaCalabretto GiuliaBuson ElenaCaregari AlbertoVicenzetto CristinaBarilà GregorioRoncaglia EleonoraMerlo RobertoTrentin LivioFacco MonicaPavan LauraSemenzato GianpietroGaffo EnricoTeramo AntonellaZambello RenatoBortoluzzi Stefania - Within a prospective cohort of patients with immune dysregulation, we identified several individuals with chronically increased proportions of TCR γδ cells but normal peripheral lymphocyte counts. Among those, we identified one individual with a TCR γδ cell-specific heterozygous p.Y665F STAT5B gain-of-function mutation. Recurrent oral aphthous lesions, susceptibility to infection, arthralgia, and fatigue, were linked to relatively elevated numbers of γδ T cells expressing a Vγ9Vδ2 TCR, displaying hyperphosphorylation of STAT5 upon in vitro IL-2 stimulation. The TCR Vγ9Vδ2 cells exhibited enhanced proliferative response to (E)-4-hydroxy-3-methyl-but-2-enyl pyrophosphate and dysregulated cytokine production. The TCR γδ cell transcriptome revealed the suppression of the default Th17 program, along with inhibition of and expression. The JAK inhibitor baricitinib improved clinical features of the observed immune dysregulation and reduced the frequency of peripheral TCR Vγ9Vδ2 cells. Thus, functionally altered TCR γδ cells may underlie chronic immune dysregulation of unknown molecular cause, demonstrated here to be amenable to tailored immune modulation. - Source: PubMed
Publication date: 2026/08/10
Meyer Benedikt JLoureiro José PedroNosi VladimirHupfer RobinGhosh AdhidebPoletti FabioJauch AnnaïseHirsiger JuliaBerkemeier CarolineHeijnen IngmarDirks JanAlborelli IlariaMenter ThomasTzankov AlexandarHess ChristophNavarini Alexander ABerger Christoph TMori LuciaDe Libero GennaroRecher Mike - STAT5B (signal transducer and activator of transcription 5B) deficiency is a rare autosomal recessive syndrome characterized by severe postnatal growth retardation, atopic dermatitis, and hormonal and immunological abnormalities. We present the case of a 7-month-old male patient with no significant perinatal history who was referred to our clinic for a skin condition that had been present for 5 months, associated with severe growth retardation (low weight for height). After ruling out the most common causes of early-onset atopic dermatitis (such as food allergies, primary immunodeficiencies, and inborn errors of metabolism), genetic testing was performed, leading to a diagnosis of STAT5B deficiency. Our objective is to present a patient with a very rare disease that has a highly characteristic presentation, thereby aiding in early diagnosis. - Source: PubMed
Publication date: 2026/08/06
Zone JulietaBuján María MCrespo CarolinaCervini Andrea B