Ask about this productRelated genes to: JAK2 antibody
- Gene:
- JAK2 NIH gene
- Name:
- Janus kinase 2
- Previous symbol:
- -
- Synonyms:
- JTK10
- Chromosome:
- 9p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-04-16
- Date modifiied:
- 2019-04-23
Related products to: JAK2 antibody
Related articles to: JAK2 antibody
- To investigate the role of ST3 β-galactoside α-2,3-sialyltransferase 1 (ST3Gal1) and vascular endothelial growth factor receptor 2 (VEGF-R2) in endometrioid-type epithelial ovarian cancer (E-OC) because aberrant α2,3-sialylation mediated by ST3Gal1 and VEGF-R2-related angiogenesis is linked with tumor progression. - Source: PubMed
Publication date: 2026/05/04
Chao Wei-TingLiu Chia-HaoYang Szu-TingLin Chen-HaoWang Liang-WeiWang Peng-Hui - Effective cancer immunotherapy requires not only efficient antigen delivery to dendritic cells (DCs) but also overcoming local immunosuppression. Here, we introduce a nanobody-LNP platform that achieves both targeting and active relicensing of DCs. By decorating lipid nanoparticles with nanobodies against the DC surface protein Plastin-2 (PLS2), our platform achieves a remarkable 93% internalization efficiency. This preferential targeting dramatically enhances antigen expression while simultaneously relicensing DCs toward a more potent, mature phenotype by inhibiting the immunosuppressive Leptin-JAK2-STAT3 signaling pathway. This integrated strategy unleashed potent cytotoxic T lymphocyte responses and led to marked inhibition of established tumors. Our work establishes PLS2 as a novel immunomodulatory receptor and presents a dual-action delivery platform that significantly boosts cancer vaccine potency. - Source: PubMed
Publication date: 2026/05/04
Qin ShugangHuang ZhiyingHuang HaiZhang YupeiChen YutingHe XiNiu ZhenyiXiang ZhongzhengZou ChaoyuSong Xiangrong - Liver fibrosis results from an imbalance between the deposition and the degradation of the extracellular matrix in the liver, for which there are currently no effective therapeutic drugs available. In this study, we demonstrated that baicalin, a major active component of the traditional Chinese medicine , was able to inhibit the activation of hepatic stellate cells and attenuate liver fibrosis in various mouse models. In order to elucidate the molecular basis of its antifibrotic effects, we designed a novel baicalin photo-cross-linking probe and applied a quantitative chemoproteomic strategy based on dimethyl labeling to profile baicalin-interacting proteins. Aided by systematic gene knockouts of these potential baicalin interactors, we identified STAT3 as a key target in mediating the antifibrotic function of baicalin. Mechanistically, baicalin primarily binds to the N-terminal domain of STAT3, inhibits its interaction with JAK2 and thereby suppresses STAT3 phosphorylation. Our findings reveal the molecular mechanism of the antifibrotic effects of baicalin and provide a theoretical basis for the design of new antifibrotic drugs based on the structure of baicalin. - Source: PubMed
Publication date: 2026/02/16
Yuan ShouliZhou Yuan-FeiMa BinLiu YuanZhang JinWang YanqiXiao WeidiLiu HaifanWang FengzhangYu AnqiYang WeipengWang Chu - Myeloproliferative neoplasms (MPN) are hematological disorders driven by mutated hematopoietic stem cells, characterized by an increased risk of thrombosis and progression to leukemia. Patients with MPN exhibit elevated levels of inflammatory factors, which function as promoters of disease progression and transformation into acute leukemia. Fufang Huangbo formula (FHF) is a classic traditional Chinese herbal medicine widely used in the treatment of inflammation-related diseases, where it has shown considerable therapeutic efficacy. However, its potential effects on MPNs remain unclear. In this study, we demonstrate for the first time across multiple animal models that FHF significantly alleviates MPN progression, including EPO-induced polycythemia vera (PV)-like, JAK2-driven PV, and MPL-driven essential thrombocythemia (ET) models. FHF effectively reduced erythrocyte aggregation-induced thrombosis in PV and reversed myelofibrosis in ET. To explore the therapeutic effects, active components, and mechanisms of FHF in MPNs, we performed network pharmacology and RNA-seq analyses, with subsequent experimental validation. The results indicate that the therapeutic benefits of FHF are closely associated with cellular senescence and inflammatory responses. Validation experiments showed that FHF induces cellular senescence via activation of the p53/p21 pathway and suppresses inflammation by inhibiting the STAT3 and NF-κB signaling pathways. Our study provides scientific evidence supporting the use of FHF in the treatment of MPNs. - Source: PubMed
Publication date: 2026/04/16
Liu MingjieLi YanxiaQin ChengxueWang LinglingGuo MeiqiWang YiZhou QianShi ZhidaHao WeiminLi YuanZhao Baobing - Suppressor of Cytokine Signaling 3 (SOCS3) is a pivotal negative regulator of the JAK/STAT pathway, and its loss or silencing is frequently associated with hyperactivated STAT3 signaling in aggressive cancers, including Triple-Negative Breast Cancer (TNBC). In this study, we present the rational design, biophysical characterization, and cellular evaluation of novel SOCS3-derived peptidomimetics that incorporate a hitherto unexploited structural determinant of the SOCS3/JAK2/Gp130 interface: the BC loop. The synthesis of individual and chimeric peptides was guided by structural analysis of the ternary complex, which combined the KIR/ESS regions with a stabilized BC loop. The results of the study revealed that the chimeric construct, KIRESS BC loop-chim, exhibited markedly improved affinity for JAK2 ( ∼ 10 μM) in comparison to the affinity of the isolated regions. This was determined by means of MicroScale Thermophoresis (MST). Circular dichroism (CD) and fluorescence spectroscopy demonstrated that turn-inducing motifs stabilize native-like conformations, correlating with enhanced serum stability. To preliminarily evaluate potential cellular effects, we assessed their serum stabilities and their cytotoxicity in MDA-MB-231 and MDA-MB-468 cells once conjugated to a small Cell-Penetreting Peptide (CPP). In both cases, the good biocompatibility of the designed mimetics appeared promising for evaluating signaling-dependent effects. These findings validate a multiregion, structure-guided design strategy and identify an improved SOCS3 proteomimetic scaffold with potential for targeting dysregulated JAK/STAT signaling in cancer. - Source: PubMed
Publication date: 2026/04/13
Cugudda AlessiaLa Manna SaraBucciero CandidaCastellano GiulianoMalfitano Anna MariaMarasco Daniela