mProX™ Human TXK Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 A decrease in oxidative stress following OGD/R stimulation is observed when Txk is subjected to knockdown.
Control, OGD/R, Txk-shRNA, and control-shRNA groups were subjected to MDA, GSH, GSH-PX, CAT, SOD, and cytochrome C activity assays, with n=6 per group. Significantly elevated MDA levels were observed in the OGD/R group compared to the control group (P<0.05), while the Txk-shRNA group exhibited reduced MDA levels compared to the OGD/R group (P<0.05). These observations highlight the impact of Txk tyrosine kinase suppression through shRNA on oxidative stress parameters in the context of oxygen and glucose deprivation/reperfusion injury, implicating potential therapeutic implications for mitigating cellular damage.
Ref: Xu, Qian-Lan, and Jie Wu. "Effects of Txk‑mediated activation of NF‑κB signaling pathway on neurological deficit and oxidative stress after ischemia‑reperfusion in rats." Molecular Medicine Reports 24.1 (2021): 1-10.
Pubmed: 34036382
DOI: 10.3892/mmr.2021.12163
Research Highlights
Martin, David A., et al. "Target Occupancy and Functional Inhibition of JAK3 and TEC Family Kinases by Ritlecitinib in Healthy Adults: an Open-Label, Phase 1 Study." The Journal of Clinical Pharmacology (2023).
Ritlecitinib is a small molecule currently undergoing clinical development, which has shown promising results in the inhibition of Janus kinase 3 (JAK3) and the TEC family of kinases (BTK, BMX, ITK, TXK, and TEC). In this study, conducted on healthy participants aged 18-60 years, the target occupancy and functional effects of ritlecitinib on JAK3 and TEC family kinases were assessed. Subjects were given single doses of 50 or 200 mg of ritlecitinib on day 1, and blood samples were collected over 48 hours to measure pharmacokinetics, target occupancy, and pharmacodynamics. Target occupancy was evaluated using mass spectroscopy, while functional inhibition was measured by the inhibition of downstream targets such as signal transducer and activator of transcription 5 (pSTAT5) for JAK3-dependent signaling and cluster of differentiation 69 (CD69) for BTK-dependent signaling. Eight participants received 50 mg and eight received 200 mg of ritlecitinib. Plasma exposure for ritlecitinib increased in a dose-proportional manner, with both doses exhibiting high levels of target occupancy for JAK3 and TEC kinases. Additionally, ritlecitinib effectively reduced pSTAT5 levels and CD69 upregulation in a dose-dependent manner, indicating dual inhibition of both pathways. Further research is needed to fully understand the therapeutic potential of ritlecitinib in targeting these pathways.
Martin, David A., et al. "Target Occupancy and Functional Inhibition of JAK3 and TEC Family Kinases by Ritlecitinib in Healthy Adults: an Open-Label, Phase 1 Study." The Journal of Clinical Pharmacology (2023).
Pubmed:
37691236
DOI:
10.1002/jcph.2347
