EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72172_C
MEK/ERK 通路抑制剂；抑制 MEK1 和 MEK2
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总览
PD98059 是一种选择性、可穿透细胞的 MEK/ERK 通路抑制剂，其作用机制为阻止上游激酶激活 MEK1（IC₅₀ = 2 - 7 µM）和 MEK2（IC₅₀ = 50 µM）。它不抑制激活的 MEK 或 p38 MAPK 通路。（Alessi et al., Davies et al., Dudley et al.）
维护和自我更新
·增强小鼠胚胎干细胞 (ES) 的生长和自我更新（Burdon et al., Qi et al.）。
·允许从难以处理的 CBA 小鼠品系中分离小鼠 ES 细胞（Buehr and Smith）。
分化
·抑制小鼠 ES 细胞分化（Burdon et al.）。
·增强人间充质干细胞的脂肪形成分化并阻止其成骨分化 （Jaiswal et al.）。
癌症研究
·减少 AML 母细胞集落的数量，对正常造血祖细胞的影响极小（Milella et al.）。
别名
不适用
细胞类型
脂肪细胞，癌细胞及细胞系，白血病/淋巴瘤细胞，间充质干/祖细胞，多能干细胞
种属
人，小鼠，非人灵长类，其他物种，大鼠
应用
分化，扩增，培养
研究领域
癌症，干细胞生物学
CAS 编号
167869-21-8
化学式
C₁₆H₁₃NO₃
分子量
267.3 g/mol
纯度
≥98%
通路
MEK/ERK
靶点
MEK
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 (3)
文献 (8)
Suppression of SHP-2 and ERK signalling promotes self-renewal of mouse embryonic stem cells.
Developmental biology 1999 JUN
Abstract
The propagation of pluripotent mouse embryonic stem (ES) cells depends on signals transduced through the cytokine receptor subunit gp130. Signalling molecules activated downstream of gp130 in ES cells include STAT3,the protein tyrosine phosphatase SHP-2,and the mitogen-activated protein kinases,ERK1 and ERK2. A chimaeric receptor in which tyrosine 118 in the gp130 cytoplasmic domain was mutated did not engage SHP-2 and failed to activate ERKs. However,this receptor did support ES cell self-renewal. In fact,stem cell colonies formed at 100-fold lower concentrations of cytokine than the unmodified receptor. Moreover,altered ES cell morphology and growth were observed at high cytokine concentrations. These indications of deregulated signalling in the absence of tyrosine 118 were substantiated by sustained activation of STAT3. Confirmation that ERK activation is not required for self-renewal was obtained by propagation of pluripotent ES cells in the presence of the MEK inhibitor PD098059. In fact,the growth of undifferentiated ES cells was enhanced by culture in PD098059. Thus activation of ERKs appears actively to impair self-renewal. These data imply that the self-renewal signal from gp130 is a finely tuned balance of positive and negative effectors.
Adult human mesenchymal stem cell differentiation to the osteogenic or adipogenic lineage is regulated by mitogen-activated protein kinase.
The Journal of biological chemistry 2000 MAR
Abstract
Adult human mesenchymal stem cells are primary,multipotent cells capable of differentiating to osteocytic,chondrocytic,and adipocytic lineages when stimulated under appropriate conditions. To characterize the molecular mechanisms that regulate osteogenic differentiation,we examined the contribution of mitogen-activated protein kinase family members,ERK,JNK,and p38. Treatment of these stem cells with osteogenic supplements resulted in a sustained phase of ERK activation from day 7 to day 11 that coincided with differentiation,before decreasing to basal levels. Activation of JNK occurred much later (day 13 to day 17) in the osteogenic differentiation process. This JNK activation was associated with extracellular matrix synthesis and increased calcium deposition,the two hallmarks of bone formation. Inhibition of ERK activation by PD98059,a specific inhibitor of the ERK signaling pathway,blocked the osteogenic differentiation in a dose-dependent manner,as did transfection with a dominant negative form of MAP kinase kinase (MEK-1). Significantly,the blockage of osteogenic differentiation resulted in the adipogenic differentiation of the stem cells and the expression of adipose-specific mRNAs peroxisome proliferator-activated receptor gamma2,aP2,and lipoprotein lipase. These observations provide a potential mechanism involving MAP kinase activation in osteogenic differentiation of adult stem cells and suggest that commitment of hMSCs into osteogenic or adipogenic lineages is governed by activation or inhibition of ERK,respectively.
Specificity and mechanism of action of some commonly used protein kinase inhibitors.
The Biochemical journal 2000 OCT
Abstract
The specificities of 28 commercially available compounds reported to be relatively selective inhibitors of particular serine/threonine-specific protein kinases have been examined against a large panel of protein kinases. The compounds KT 5720,Rottlerin and quercetin were found to inhibit many protein kinases,sometimes much more potently than their presumed targets,and conclusions drawn from their use in cell-based experiments are likely to be erroneous. Ro 318220 and related bisindoylmaleimides,as well as H89,HA1077 and Y 27632,were more selective inhibitors,but still inhibited two or more protein kinases with similar potency. LY 294002 was found to inhibit casein kinase-2 with similar potency to phosphoinositide (phosphatidylinositol) 3-kinase. The compounds with the most impressive selectivity profiles were KN62,PD 98059,U0126,PD 184352,rapamycin,wortmannin,SB 203580 and SB 202190. U0126 and PD 184352,like PD 98059,were found to block the mitogen-activated protein kinase (MAPK) cascade in cell-based assays by preventing the activation of MAPK kinase (MKK1),and not by inhibiting MKK1 activity directly. Apart from rapamycin and PD 184352,even the most selective inhibitors affected at least one additional protein kinase. Our results demonstrate that the specificities of protein kinase inhibitors cannot be assessed simply by studying their effect on kinases that are closely related in primary structure. We propose guidelines for the use of protein kinase inhibitors in cell-based assays.
更多信息
| Molecular Weight | 267.3 g/mol |
|---|---|
| 物种 | 人, 其它物种, 大鼠, 小鼠, 非人灵长类 |
| Alternative Names | Not applicable |
| Cas Number | 167869-21-8 |
| Chemical Formula | C₁₆H₁₃NO₃ |
| 纯度 | ≥ 98% |
| Target | MEK |
| Pathway | MEK/ERK |
质量保证:
产品仅供研究使用，不用于针对人或动物的诊断或治疗。
产品仅供研究使用，不用于针对人或动物的诊断或治疗。
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