EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72152_C
PI3K/AKT通路抑制剂；抑制PI3K
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总览
LY294002 是一种 PI3K 抑制剂，其效力和选择性均高于其结构基础槲皮素。LY294002 可抑制 PI3K（IC₅₀ = 1.4 µM），并且对 CK2 也具有活性，但对 PI4K、EGFR、PDGFR、MAPK、PKA 或 PKC 无活性。（Davies et al., Vlahos et al.）
维持和自我更新
·抑制小鼠胚胎干细胞 (ES) 的增殖和自我更新（Lianguzova et al., Paling et al.）。
分化
·促进小鼠 ES 细胞分化为胰岛素分泌细胞（Hori et al.）。
·抑制成肌细胞形成肌管（Coolican et al., Jiang et al.）。
别名
不适用
细胞类型
内胚层，PSC衍生，肌源干/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
研究领域
神经科学，干细胞生物学
CAS 编号
154447-36-6
化学式
C₁₉H₁₇NO₃
分子量
307.3 g/mol
纯度
≥98%
通路
PI3K/AKT
靶点
PI3K
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 (7)
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.
Regulation of embryonic stem cell self-renewal by phosphoinositide 3-kinase-dependent signaling.
The Journal of biological chemistry 2004 NOV
Abstract
The maintenance of murine embryonic stem (ES) cell self-renewal is regulated by leukemia inhibitory factor (LIF)-dependent activation of signal transducer and activator of transcription 3 (STAT3) and LIF-independent mechanisms including Nanog,BMP2/4,and Wnt signaling. Here we demonstrate a previously undescribed role for phosphoinositide 3-kinases (PI3Ks) in regulation of murine ES cell self-renewal. Treatment with the reversible PI3K inhibitor,LY294002,or more specific inhibition of class I(A) PI3K via regulated expression of dominant negative Deltap85,led to a reduction in the ability of LIF to maintain self-renewal,with cells concomitantly adopting a differentiated morphology. Inhibition of PI3Ks reduced basal and LIF-stimulated phosphorylation of PKB/Akt,GSK3alpha/beta,and S6 proteins. Importantly,LY294002 and Deltap85 expression had no effect on LIF-induced phosphorylation of STAT3 at Tyr(705),but did augment LIF-induced phosphorylation of ERKs in both short and long term incubations. Subsequently,we demonstrate that inhibition of MAP-Erk kinases (MEKs) reverses the effects of PI3K inhibition on self-renewal in a time- and dose-dependent manner,suggesting that the elevated ERK activity observed upon PI3K inhibition contributes to the functional response we observe. Surprisingly,upon long term inhibition of PI3Ks we observed a reduction in phosphorylation of beta-catenin,the target of GSK-3 action in the canonical Wnt pathway,although no consistent alterations in cytosolic levels of beta-catenin were observed,indicating this pathway is not playing a major role downstream of PI3Ks. Our studies support a role for PI3Ks in regulation of self-renewal and increase our understanding of the molecular signaling components involved in regulation of stem cell fate.
Phosphoinositide 3-kinase inhibitor LY294002 but not serum withdrawal suppresses proliferation of murine embryonic stem cells.
Cell biology international 2007 APR
Abstract
Mouse embryonic stem (mES) cells have short duration of their cell cycle and are capable of proliferating in the absence of growth factors. To find out which signaling pathways contribute to the regulation of the mES cell cycle,we used pharmacological inhibitors of MAP and PI3 kinase cascades. The MAP kinase inhibitors as well as serum withdrawal did not affect mES cell cycle distribution,whereas the inhibitor of PI3K activity,LY294002,induced accumulation of cells in G(1) phase followed by apoptotic cell death. Serum withdrawal also causes apoptosis,but it does not change the content and activity of cell cycle regulators. In contrast,in mES cells treated with LY294002,the activities of Cdk2 and E2F were significantly decreased. Interestingly,LY294002had a much stronger effect on cell cycle distribution in low serum conditions,implying that serum can promote G(1)--textgreaterS transition of mES cells by a LY294002-resistant mechanism. Thus,proliferation of mES cells is maintained by at least two separate mechanisms: a LY294002-sensitive pathway,which is active even in the absence of serum,and LY294002-resistant,but serum-dependent,pathway.
更多信息
| Molecular Weight | 307.3 g/mol |
|---|---|
| 物种 | 人, 其它物种, 大鼠, 小鼠, 非人灵长类 |
| Alternative Names | Not applicable |
| Cas Number | 154447-36-6 |
| Chemical Formula | C₁₉H₁₇NO₃ |
| 纯度 | ≥ 98% |
| Target | PI3K |
| Pathway | PI3K/AKT |
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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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