Anti-Human CD127 PE 100 tests
- Known as:
- Antibody toHuman CD127 PE 100 tests
- Catalog number:
- 12-1278-73
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD127 100 tests
Related genes to: Anti-Human CD127 PE 100 tests
- Gene:
- IL7R NIH gene
- Name:
- interleukin 7 receptor
- Previous symbol:
- -
- Synonyms:
- CD127, IL7RA
- Chromosome:
- 5p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-07
- Date modifiied:
- 2019-04-23
Related products to: Anti-Human CD127 PE 100 tests
Related articles to: Anti-Human CD127 PE 100 tests
- Living cell therapies lack robust, reversible mechanisms for externally controlling therapeutic activity after administration, limiting their safety and clinical adaptability. Here we engineer a drug-gated cellular immunotherapy platform in which T cells function as programmable factories that secrete two inactive antibody modules whose extracellular assembly into a functional bispecific T cell engager (TCE) is controlled by a small-molecule input. Using a rapalog-inducible FKBP-FRB* heterodimerization switch, we design a split CD19 × CD3 engager architecture that remains inactive in the absence of drug and assembles on demand upon rapalog exposure. A 2A-peptide bicistronic construct enables coordinated expression and secretion of both modules, allowing precise drug-dependent control of TCE formation in situ. Drug administration quantitatively regulates T cell activation and cytotoxicity against CD19 targets in vitro, with stringent OFF-state behavior in the absence of rapalog. In xenograft models, systemic rapalog administration induces on-demand anti-tumor activity without evidence of treatment-related toxicity, demonstrating reversible pharmacological control of a locally secreted therapeutic interface. We further extend this strategy to an EGFR-targeting TCE, demonstrating the modularity and broad adaptability of the platform across distinct antigen specificities. This work introduces a generalizable engineering framework for externally programmable cell therapies, enabling tunable, safety-by-design control of T cell-based immunotherapies. - Source: PubMed
Publication date: 2026/08/24
Luengo-Arias SusanaDomínguez-Alonso CarmenZagorac IvanaTapia-Galisteo AntonioGarcía-Veros EvaRubio-Pérez LauraGómez-Rosel MarinaFuentes PatriciaHernández-López PatriciaAguilar-Sopeña ÓscarAlmagro-Puente LauraMartínez-González SoniaCañizares-Moscato LucíaRivas-Sánchez MaríaBlanco BelénRamírez-Fernández ÁngelDíez-Alonso LauraBlanco-Aparicio CarmenArroyo-Ródenas JavierMartínez-Torrecuadrada JorgeToribio María LRoda-Navarro PedroJiménez-Reinoso AnaïsÁlvarez-Vallina Luis - Meningiomas are common intracranial tumors lacking effective chemotherapeutic options. Momordicine I, a triterpenoid isolated from bitter melon, has demonstrated anticancer activity, but its effects on meningioma remain unclear. The effect of Momordicine I on meningiomas is studied in this research. - Source: PubMed
Publication date: 2026/08/10
Kao YingHu Jia-RongYang Fu-ChiHueng Dueng-YuanTsai Chia-Kuang - Cardiovascular events such as myocardial infarction (MI) show an early morning peak, suggesting circadian regulation of cardiac vulnerability. However, the mechanisms through which sleep loss may contribute to time-of-day myocardial risk remain unclear. We examined whether insomnia-associated circadian and thrombotic alterations are associated with morning cardiac vulnerability. Rats were subjected to pharmacologically induced insomnia using -chlorophenylalanine (PCPA), isoproterenol-induced myocardial stress, and their combination. Temporal profiling across zeitgeber times (ZTs) assessed locomotor activity, biochemical markers (melatonin, serotonin, and cardiac troponin I), cardiac electrophysiology, and coagulation parameters. Integrative transcriptomic analysis was performed using human insomnia and MI data sets. Experimentally, insomnia and myocardial stress altered rest-activity, temporal electrophysiology, biochemical, and coagulation circadian profiles, and the combined condition showed the most pronounced alterations. These included changes in cardiac conduction and repolarization indices, altered melatonin rhythmicity, altered serotonin levels, elevated troponin I, reduced clotting time, and increased platelet aggregation, predominantly during ZT6-ZT12, corresponding to the light-dark transition, analogous to the human early morning phase. PCPA effects were restricted to the light phase, whereas ISO-containing groups showed sustained alterations. Integrative transcriptomic analysis identified a candidate circadian-thrombotic molecular signature involving CRY1, F2R, LEP, SSTR2, and IL7R, with mRNA profiling in rats showing altered Cry1 expression in heart and Lep expression in both SCN and the heart, suggesting altered SCN-heart coordination under combined insomnia and MI. These findings suggest a shift toward a pro-thrombotic cardiac profile during the early day window with insomnia-associated circadian alterations, supporting future investigation of circadian-informed chronotherapeutic approaches for morning cardiac vulnerability. - Source: PubMed
Publication date: 2026/07/31
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Publication date: 2026/08/17
Snow Timothy Arthur ChandosCharoenpong SunnyKim HaeunCarthigesan KeshavaGallagher LauraElkhodair SamerAvraham RoiDas AbhishekSinger MervynBrealey DavidArulkumaran Nishkantha - Calcific aortic valve disease (CAVD) is an active, cell-mediated disorder lacking effective medical therapy. The contribution of programmed cell death (PCD) to disease progression remains insufficiently characterized. This study aimed to characterize PCD-related transcriptomic features during CAVD progression and identify candidate molecular indicators associated with disease severity. - Source: PubMed
Publication date: 2026/06/23
Yu XianguanZhao YunyueChen ZefengTang LeileXiong Zhaojun