Anti-Mouse CD127 FITC 50 ug
- Known as:
- Antibody toMouse CD127 fluorecein 50 ug
- Catalog number:
- 11-1271-81
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD127 FITC 50
Related genes to: Anti-Mouse CD127 FITC 50 ug
- 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-Mouse CD127 FITC 50 ug
Related articles to: Anti-Mouse CD127 FITC 50 ug
- 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
Kumar NeerajSiddiqui Mohammad AquibKrishnamurthy Sairam - Sepsis is associated with immunosuppression, predisposing patients to secondary infections. Many treatments routinely used for infections have immunomodulatory effects, including antibiotics. We therefore assessed the immunomodulatory effects of beta-lactam antibiotics on monocyte and lymphocyte immunophenotype. - Source: PubMed
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 - Dermal group 2 innate lymphoid cells (dILC2s) contribute to skin homeostasis and inflammatory responses, yet they are frequently studied in Rag1-deficient mice in which the dILC2 compartment may itself be altered. - Source: PubMed
Publication date: 2026/07/20
Saleh Mohamed MLiao KexinBraun AndreaSalinas GabrielaSchön Michael PDasari PrasadBuhl Timo - Regulatory CD4+ T cells (Tregs), as defined by expression of the transcription factor Foxp3, strongly depend on the cytokine interleukin 2 (IL-2) for their survival and function and are often identified by the combination of high IL-2Rα (CD25) and low IL-7Rα (CD127) expression. Nevertheless, subsets expressing higher levels of IL-7Rα have been described, and IL-7 signaling does play a role in Treg function in some specific biologic contexts and tissues. The precise role of IL-7Rα-expressing Tregs in autoimmunity remains poorly defined though, potentially hampering current efforts to develop IL-7Rα blockade for the treatment of various autoimmune diseases. To ask whether cell-intrinsic IL-7Rα expression in Tregs was required for their function during type 1 diabetes (T1D) development, we generated non-obese diabetic (NOD) mice in which IL-7Rα is exclusively deleted in Foxp3-expressing Tregs. In young NOD mice, IL-7Rα deficiency did not alter Treg numbers and phenotype. However, 100% of NOD mice with IL-7Rα-deficient Tregs became diabetic, while the T1D incidence is typically around 50-60% in our colony. This increased susceptibility for T1D indicates that IL-7Rα expression in Tregs is required to protect a subset of NOD mice against islet autoimmunity. At the time of T1D onset, CD4+ and CD8+ T cells from NOD mice with IL-7Rα-deficient Tregs showed increased IFN-γ and IL-2 cytokine production. Our data demonstrate that cell-intrinsic IL-7R signaling in Foxp3+ Tregs is required to suppress effector T cell responses and to prevent full penetrance of T1D in NOD mice. - Source: PubMed
Jones Iv Albert RSmith Peyton SDooms Hans