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
- : 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 - Stem cell factor (SCF), also known as Kit ligand, is a pleiotropic cytokine that signals through the c-Kit receptor to regulate cellular development, survival, and proliferation. Although SCF is classically recognized for its essential role in hematopoiesis and mast cell biology, c-Kit is also expressed by innate lymphoid cell progenitors (ILCp) and subsets of mature innate lymphoid cells (ILCs), suggesting broader immunoregulatory functions. Group 2 innate lymphoid cells (ILC2s) are critical mediators of type 2 airway inflammation and serve as an important source of type 2 cytokines during allergic responses. We previously demonstrated increased expression of the pro-inflammatory SCF248 isoform in the lungs of mice with chronic allergic inflammation, while elevated soluble SCF levels have also been reported in patients with asthma. In the present study, we further observed that SCF248 is upregulated in the bone marrow during allergic inflammation, suggesting that SCF248 may contribute to both local and systemic regulation of allergic immune responses. To define the role of SCF/c-Kit signaling in ILC2 biology, we first performed transcriptional profiling of SCF-deficient ILC2s, which revealed reduced expression of genes associated with cytokine signaling, activation, and effector function, including , , and pathway components, consistent with impaired inflammatory responsiveness. Mechanistically, pro-inflammatory and type 2 cytokines induced SCF248 expression in mesenchymal cells . To define its functional impact, ILC progenitors were cultured on OP9-DL1 stromal cells with upregulated SCF248 expression, which increased expression of ILC2-associated markers and the maturation program, supporting a role for SCF248 in enhancing ILC2 maturation and activation. validation using tamoxifen-inducible whole-body SCF-deficient mice (SCF UBC-CreERT2) in an model of allergic airway inflammation demonstrated that SCF deficiency reduced SCF248 expression, attenuated type 2 cytokine production, diminished lung inflammation, and decreased circulating and pulmonary ILC2 populations. Similarly, SCF248 blockade reduced allergic inflammation and altered bone marrow ILC compartments. Together, these findings identify SCF248 as a regulator of ILC2 maturation and activation, amplifying mucosal type 2 inflammation during allergic airway disease. - Source: PubMed
Publication date: 2026/07/02
Asai NobuhiroLombardo Grace KOcadiz-Ruiz RamonGu YaoRasky Andrew JGarcia Dana SMontoya Angela JMontaño SaritaYagi KazumaFonseca Wendy - Autophagy is an ancient catabolic process that has emerged as part of innate immunity. Upon infection, autophagy is activated but the key factors responsible remained unclear. Here, we show that interferon (IFN) released during viral infections subsequently activates autophagy via STAT1/5B-mediated upregulation of Suppressor of Cytokine Signaling 1 (SOCS1). Our data show that scavenging of IFNs diminishes autophagy induced by several respiratory viruses. All types of IFN (I, II and III) mediated robust autophagic flux activation in both cell lines and primary human lung fibroblasts in a JAK1-3 dependent manner. Depletion or pharmacological inhibition of individual signal transducer and activator of transcription (STAT) transcription factors demonstrated that both STAT1 and STAT5B are required for IFN-induced autophagy. Upon IFN stimulation STAT1 and STAT5B associate and translocate to the nucleus. Transcriptome analyses revealed that most known anti-viral IFN-stimulated genes (ISGs) remain induced to high levels upon inhibition of STAT5 expect for a small subset of ISGs, among them SOCS1. Overexpression of SOCS1 stimulated autophagy, whereas its depletion impaired IFN-induced autophagy. Successful viruses like measles virus (MeV) or respiratory syncytial virus (RSV) evolved strategies to exploit autophagy to promote their own replication. Uncoupling IFN-mediated ISG defenses from autophagy induction by STAT5 inhibition reduced virus-induced autophagy, and inhibited efficient replication of autophagy-dependent MeV and RSV. Overexpression of SOCS1 upon STAT5 inhibition largely rescued both infection-induced autophagy and viral replication. Taken together, our data show that IFN promotes autophagy via STAT1/STAT5B-SOCS1 in viral infections and reveal that targeting of this axis allows inhibition of autophagy-dependent viruses without compromising innate immune defenses. - Source: PubMed
Publication date: 2026/07/15
Hunszinger VictoriaKlute SusanneEngels ZoéHoenigsperger HeleneKoepke LennartDürr HelenFischer Jana-RomanaOtt BirgitGraf AlexanderKrebs StefanBlum HelmutKirchhoff FrankHirschenberger MaximilianSparrer Konstantin M J