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
- Colorectal cancer (CRC) resistance to 5-fluorouracil (5-FU), primarily driven by cancer stem cells (CSCs) and epithelial-mesenchymal transition (EMT), remains a major clinical challenge, necessitating novel therapeutic strategies. - Source: PubMed
Publication date: 2025/04/16
Wen ChengliZhang XuKantapan JirapornYu ZehuiYuan LipingLiu ShaLi HaoLiang SichengWei YanLuo GangXiao WanmengDechsupa NathupakornLü Muhan - Globally, lung cancer is the primary cause of deaths associated with cancer; however, current therapies are costly and toxic, highlighting the need for novel treatments. Peiminine (Verticinone), a key bioactive compound derived from Maxim., has demonstrated diverse biological activities. However, the precise pharmacological mechanisms underlying its anti-lung cancer effects remain unclear. The objective of this study was to quantify the content of peiminine in Maxim. from different geographical regions using UHPLC-MS/MS and to elucidate the anti-lung cancer mechanisms of peiminine through network pharmacology, bioinformatics, and in vitro experiments. The content of peiminine in Maxim. from various regions was determined using UHPLC-MS/MS. Potential target genes associated with peiminine and lung cancer were systematically screened from multiple databases. To identify core genes, we set up a PPI (protein-protein interaction) network, followed by in-depth analyses of their corresponding target proteins. Survival analysis, molecular docking, and dynamics simulations were used to explore potential anti-cancer mechanisms. In vitro experiments on human H1299 NSCLC cells assessed peiminine's anti-tumor activity and measured key gene transcription levels. UHPLC-MS/MS analysis revealed that Maxim. from Mudanjiang (Heilongjiang Province) exhibited the highest peiminine content. Network pharmacological analysis identified PIK3CG, SRC, JAK3, AKT2, and PRKCA as key potential targets of peiminine in lung cancer treatment. Molecular docking results demonstrated strong binding affinities between peiminine and PIK3CG, SRC, and JAK3; these results were further confirmed using molecular dynamics simulations. Survival analysis indicated that a high AKT2 and PRKCA expression correlated with bad prognosis in lung cancer patients. In vitro, peiminine inhibited H1299 cell viability and regulated genes involved in the PI3K-Akt pathway (PI3K, AKT, and PTEN) and apoptosis (Bcl-2, Bax), suggesting that it may induce its effects via PI3K-Akt pathway inhibition. Peiminine from Maxim. exhibits significant anti-lung cancer potential by targeting key genes such as PIK3CG, SRC, and JAK3, as well as by modulating the PI3K-Akt signaling pathway and apoptosis-related genes. These results lay a foundation for further investigations into peiminine as a potentially effective therapeutic option for treating lung cancer. Additionally, the identified targets (PIK3CG, SRC, JAK3, AKT2, and PRKCA) may function as possible biomarkers for predicting lung cancer prognosis and guiding personalized therapy. - Source: PubMed
Publication date: 2025/04/09
Yang ZiwenSyed Faizan Ali ShahHuang XinhuiWei LinZhong YinzeShi XuepengWu XiaotianGan ChunliWang ZhibinYang Chunjuan - To assess the effect of a potent cytochrome P450 (CYP) 3A inhibitor and CYP inducer on the pharmacokinetics of ritlecitinib, a JAK3/TEC family kinase inhibitor, and assess the effect of ritlecitinib on the pharmacokinetics of CYP substrates (midazolam, efavirenz, tolbutamide, caffeine and oral contraceptives [ethinyl oestradiol and levonorgestrel]) in healthy adults. - Source: PubMed
Publication date: 2025/05/07
Purohit Vivek SHuh YeaminDowty Martin EPlotka AnnaLejeune AlexandreKalluru HinduHee Brian - JAK inhibition (JAKi) is effective in seronegative spondyloarthropathy (SpA) spectrum disorders, but TYK2 inhibition failed in SpA spectrum ulcerative colitis, and tofacitinib showed minimal benefit in Crohn's Disease, which highlights the complex role for JAK-STAT signaling in different inflammatory processes. In this study, we investigated whether JAKi might paradoxically activate entheseal innate immunity and aimed to identify the key regulatory cytokines involved in this process. - Source: PubMed
Publication date: 2025/05/05
Giryes SamiWong ChiBridgewood CharlieHarland MarkAltaie AlaMcDermott NicoleAbacar KeremRao AbhayKhan AlmasMcMillan TristanLoughenbery PeterDunsmuir RobertBorse VishalMacleod TomMcGonagle Dennis - In acute lymphoblastic leukaemia (ALL), cytoplasmic CD3 (cCD3) is a defining marker for T-lineage, and CD19 plus additional B-cell marker(s) for B-lineage. We identified 23 ALL cases in which the lymphoblasts expressed both cCD3 and CD19, making lineage assignment challenging. These cases represented approximately 10% of cCD3+ ALL and expressed a median of two additional B-cell markers other than CD19, including CD79a (76%), CD22 (22%), PAX5 (57%) and CD10 (44%). Two cases were mixed for T/B-lineage ALL, both positive for BCR::ABL1 rearrangement. In the remaining 21 cases, IgH and/or IgK/L rearrangement were detected in 1 of 19 cases and TRG/TRB in 13 of 21 (62%) cases. Other T-ALL characteristic genetic abnormalities included NOTCH1 mutations (7/21, 33%), PHF6 (6/21, 29%), JAK3 (4/21, 19%), PICALM::MLLT10, TLX3::BCL11B, TRB::HOXA13, SPTAN1::NUP214 and deletion of CDKN2A/CDKN2B. In the 16 cases that demonstrated a T-ALL genetic profile, CD22 (2/16, 13%) was found to be a more specific additional B-lineage marker than CD79a (11/15, 73%), PAX5 (8/14, 57%) or CD10 (7/16, 44%). Our data suggest that mixed T/B-ALL is extremely rare, with most cases associated with BCR::ABL1 and blast crisis of myeloproliferative neoplasms. The majority of cases represent early T-precursor lymphoblastic leukaemia expressing aberrant B-cell markers. We also showed persistent CD19 expression in relapsed/residual disease (16/17, 94%), suggesting its potential role as a therapeutic target and as a marker for detection of residual/relapse disease in these ALL cases. - Source: PubMed
Publication date: 2025/04/02
E ShuyuJelloul Fatima ZNahmod Karen AShort NicholasLeventaki VasilikiJia FuliXu JieLoghavi SanamWang WeiJabbour L EliasTang GuilinMedeiros L JeffreyWang Sa A