EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #70026_C
冻存的人原代细胞
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概览
原代人CD4+ T细胞通过使用免疫磁珠负选技术从外周血（PB）单个核细胞（MNCs）中分离获得。PB使用抗凝剂酸性柠檬酸葡萄糖溶液A（ACDA）收集。
细胞使用机构审查委员会（IRB）批准的同意书和方案获取。某些产品仅在特定国家/地区提供。
某些产品仅在特定国家/地区提供。请联系您当地的销售代表或产品与科学支持部门（邮箱：techsupport.cn@stemcell.com）以获取更多信息。
包含
• CryoStor® CS10
分类
冻存
细胞类型
T 细胞，CD4+ T细胞
物种
人
细胞和组织来源
外周血
研究领域
药物发现和毒性检测
供体状态
正常
纯度
≥ 85% CD4+（通过流式分析检测）
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。
相关材料与文献
技术资料 (4)
文献 (2)
Isoform-selective activity-based profiling of ERK signaling. Chemical science 2018 MAR
Abstract
Extracellular signal-regulated kinases (ERKs) mediate downstream signaling of RAS-RAF-MEK as key regulators of the mitogen-activated protein kinase (MAPK) pathway. Activation of ERK signaling is a hallmark of cancer and upstream MAPK proteins have been extensively pursued as drug targets for cancer therapies. However, the rapid rise of resistance to clinical RAF and MEK inhibitors has prompted interest in targeting ERK (ERK1 and ERK2 isoforms) directly for cancer therapy. Current methods for evaluating activity of inhibitors against ERK isoforms are based primarily on analysis of recombinant proteins. Strategies to directly and independently profile native ERK1 and ERK2 activity would greatly complement current cell biological tools used to probe and target ERK function. Here, we present a quantitative chemoproteomic strategy that utilizes active-site directed probes to directly quantify native ERK activity in an isoform-specific fashion. We exploit a single isoleucine/leucine difference in ERK substrate binding sites to enable activity-based profiling of ERK1 versus ERK2 across a variety of cell types, tissues, and species. We used our chemoproteomic strategy to determine potency and selectivity of academic (VX-11e) and clinical (Ulixertinib) ERK inhibitors. Correlation of potency estimates by chemoproteomics with anti-proliferative activity of VX-11e and Ulixertinib revealed that {\textgreater}90{\%} inactivation of both native ERK1 and ERK2 is needed to mediate cellular activity of inhibitors. Our findings introduce one of the first assays capable of independent evaluation of native ERK1 and ERK2 activity to advance drug discovery of oncogenic MAPK pathways.
Evidence of an oncogenic role of aberrant TOX activation in cutaneous T-cell lymphoma. Blood 2015 FEB
Abstract
TOX is a nuclear factor essential for the development of CD4(+) T cells in the thymus. It is normally expressed in low amounts in mature CD4(+) T cells of the skin and the peripheral blood. We have recently discovered that the transcript levels of TOX were significantly increased in mycosis fungoides, the most common type of cutaneous T-cell lymphoma (CTCL), as compared to normal skin or benign inflammatory dermatoses. However, its involvement in advanced CTCL and its biological effects on CTCL pathogenesis have not been explored. In this study, we demonstrate that TOX expression is also enhanced significantly in primary CD4(+)CD7(-) cells from patients with Sézary syndrome, a leukemic variant of CTCL, and that high TOX transcript levels correlate with increased disease-specific mortality. Stable knockdown of TOX in CTCL cells promoted apoptosis and reduced cell cycle progression, leading to less cell viability and colony-forming ability in vitro and to reduced tumor growth in vivo. Furthermore, TOX knockdown significantly increased 2 cyclin-dependent kinase (CDK) inhibitors, CDKN1B and CDKN1C. Lastly, blocking CDKN1B and CDKN1C reversed growth inhibition of TOX knockdown. Collectively, these findings provide strong evidence that aberrant TOX activation is a critical oncogenic event for CTCL.
更多信息
| 物种 | 人类 |
|---|---|
| Contains | • CryoStor® CS10 |
| 纯度 | ≥ 85% CD4+ by flow cytometry |
| 细胞与组织来源 | 外周血 |
| 捐献者身份 | 正常 |
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