Jak3, Active Human Recombinant Protein
- Known as:
- Jak3, Active Human Recombinant Protein
- Catalog number:
- 40452
- Product Quantity:
- 10 µg
- Category:
- -
- Supplier:
- Biotech support group
- Gene target:
- Jak3 Active Human Recombinant Protein
Related genes to: Jak3, Active Human Recombinant Protein
- Gene:
- JAK3 NIH gene
- Name:
- Janus kinase 3
- Previous symbol:
- -
- Synonyms:
- L-JAK, JAKL, LJAK, JAK3_HUMAN, JAK-3
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-19
- Date modifiied:
- 2019-04-23
Related products to: Jak3, Active Human Recombinant Protein
Related articles to: Jak3, Active Human Recombinant Protein
- While chimeric antigen receptor (CAR) T-cell therapy provides potential cure for patients with non-Hodgkin B-cell lymphomas/leukemias and plasma cell myelomas, rare reports of development of T-cell lymphomas(TCLs) in these patients have raised serious safety concerns with regard to whether CAR T-cell therapy could directly contribute to the development of TCLs in a specific patient or in those with certain types of underlying hematologic malignancy. This review aims to comprehensively evaluate the clinicodemographic features, types of TCLs, immunophenotypic characteristics, mutational profiles, and CAR-T transgene expression status within the lymphoma cells, as well as explore the underlying mechanisms of lymphomagenesis. A special focus is placed on the interplay between the pre-existing clonal hematopoiesis, immune dysregulation, and reported genomic alterations that may predispose to and/or drive T-cell lymphomagenesis. Among the total 18 reported cases, they developed in all types of underlying hematologic malignancies, and they occurred in all types of widely used commercial CAR T-cell products. The majority of the TCLs showed aberrant T-cell phenotypes according to CD4 and/or CD8 expression. The infused CAR-T transgene from lymphoma cells was detected in 63%(10/16) cases, and 73%(8/11) cases showed integration of the CAR transgene into a known tumor suppressor gene or oncogene. At the molecular genomic level, mutations involved in epigenetic regulators (TET2 and DNMT3A) and JAK-STAT signaling pathway especially JAK3 mutation, were often detected. The potential mechanisms of T-cell lymphomagenesis were complex and multifactorial including but not limited to pre-existing clonal hematopoiesis of indeterminate potential genes, malignant transformation of CAR T-cells, and lymphodepletion chemotherapy. - Source: PubMed
Publication date: 2026/08/20
Shi WangpanWang Huan-You - Post-treatment erythrocytosis (PT-E)-an increase in red blood cell counts after therapy-is an uncommon but reproducible finding in a subset of Hodgkin lymphoma (HL) survivors, and its biological basis remains undefined. - Source: PubMed
Publication date: 2026/08/05
Koyun DeryaYüksel SeherCivriz Bozdağ SinemTuncalı TimurKuzu IşınsuÖzcan Muhit - : 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 - Helicobacter pylori (H. pylori) is a major cause of chronic gastritis and gastric cancer. Macrophages are key regulators of gastric immunity, yet the mechanisms by which H. pylori reprogram macrophage activation and suppresses host immune responses remain unclear. RAW264.7 macrophages were infected with H. pylori PMSS1. Macrophage polarization, cytokine secretion, and JAK3/STAT5-SOCS3 signaling were examined by qRT-PCR, Western blotting, flow cytometry, and ELISA. Ritlecitinib was used to inhibit JAK3. Primary naive CD4⁺ T cells were treated with macrophage-conditioned medium to assess proliferation, CD25/CD69 activation, and FoxP3⁺ Treg differentiation. SOCS3 knockdown was used to evaluate rescue effects. H. pylori significantly promoted M1 macrophage polarization, with increased CD86, iNOS, MHC II, TNF-α, and IFN-γ and decreased CD163, Arg1, TGF-β, and IL-10 (p < 0.05). H. pylori also upregulated JAK3, STAT5, and SOCS3, while Ritlecitinib attenuated inflammatory gene expression (p < 0.05). Hp-CM significantly inhibited primary CD4⁺ T-cell proliferation, CD25/CD69 activation, and CD4⁺CD25⁺FoxP3⁺ Treg differentiation (p < 0.05). SOCS3 knockdown partially restored these CD4⁺ T-cell responses (p < 0.05). H. pylori promotes M1 macrophage polarization and impairs CD4⁺ T-cell immunity through JAK3/STAT5-SOCS3-mediated immune dysregulation. This mechanism contributes to chronic immune dysregulation and supports bacterial persistence, identifying JAK3/SOCS3 as potential therapeutic targets. - Source: PubMed
Publication date: 2026/08/11
Chen JianZhou LiLi LingWang Yue - In patients with locally advanced, metastatic, or recurrent nasopharyngeal carcinoma (NPC), immunotherapy, especially with programmed cell death ligand 1 (PD-L1) inhibitors, is increasingly being applied for clinical treatment and has shown promising results. Intercellular adhesion molecule 1 (ICAM1) is closely associated with the occurrence and progression of NPC induced by Epstein-Barr virus (EBV) infection and is related to the high expression of PD-L1 and immune suppression in tumour tissues. However, the specific mechanisms are unclear. - Source: PubMed
Publication date: 2026/08/11
Liu YFu RSun WChen P