EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72402_C
非肌肉肌球蛋白 II (NM II) ATPase 抑制剂
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总览
(-)-Blebbistatin是是一种选择性细胞通透性非肌肉型肌球蛋白 II ATPase 抑制剂 (Kovács et al.; Straight et al.)。它能快速且可逆地抑制多个物种的 Mg-ATPase 活性和非肌肉型肌球蛋白 IIA 和 IIB 的体外运动能力 (IC₅₀ = 0.5-5.0 μM)，而对平滑肌肌球蛋白的抑制作用较弱 (IC₅₀ = 80 μM) （Limouze et al.）。
维持和自我更新
·添加ROCK抑制剂后提高人多能干细胞（hPSC）解离为单细胞后的存活率和克隆效率（Chen et al.; Ohgushi et al.; Walker et al.; Xu et al.)。
·使 hPSC 能够在无表面涂层的微载体上培养（Chen et al.）。
·抑制人间充质干细胞的分化（McBeath et al.; Engler et al.)。
细胞类型
间充质干/祖细胞，多能干细胞
种属
人，小鼠，非人灵长类，其它细胞系，大鼠
应用
培养
研究领域
干细胞生物学
CAS 编号
856925-71-8
化学式
C₁₈H₁₆N₂O₂
纯度
≥98%
靶点
NM II ATPase
产品说明书及文档
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应用领域
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相关材料与文献
技术资料 (3)
文献 (10)
Revealing a core signaling regulatory mechanism for pluripotent stem cell survival and self-renewal by small molecules. Proceedings of the National Academy of Sciences of the United States of America 2010 MAY
Abstract
Using a high-throughput chemical screen, we identified two small molecules that enhance the survival of human embryonic stem cells (hESCs). By characterizing their mechanisms of action, we discovered an essential role of E-cadherin signaling for ESC survival. Specifically, we showed that the primary cause of hESC death following enzymatic dissociation comes from an irreparable disruption of E-cadherin signaling, which then leads to a fatal perturbation of integrin signaling. Furthermore, we found that stability of E-cadherin and the resulting survival of ESCs were controlled by specific growth factor signaling. Finally, we generated mESC-like hESCs by culturing them in mESC conditions. And these converted hESCs rely more on E-cadherin signaling and significantly less on integrin signaling. Our data suggest that differential usage of cell adhesion systems by ESCs to maintain self-renewal may explain their profound differences in terms of morphology, growth factor requirement, and sensitivity to enzymatic cell dissociation.
Non-muscle myosin II regulates survival threshold of pluripotent stem cells. Nature communications 2010 JAN
Abstract
Human pluripotent stem (hPS) cells such as human embryonic stem (hES) and induced pluripotent stem (hiPS) cells are vulnerable under single cell conditions, which hampers practical applications; yet, the mechanisms underlying this cell death remain elusive. In this paper, we demonstrate that treatment with a specific inhibitor of non-muscle myosin II (NMII), blebbistatin, enhances the survival of hPS cells under clonal density and suspension conditions, and, in combination with a synthetic matrix, supports a fully defined environment for self-renewal. Consistent with this, genetically engineered mouse embryonic stem cells lacking an isoform of NMII heavy chain (NMHCII), or hES cells expressing a short hairpin RNA to knock down NMHCII, show greater viability than controls. Moreover, NMII inhibition increases the expression of self-renewal regulators Oct3/4 and Nanog, suggesting a mechanistic connection between NMII and self-renewal. These results underscore the importance of the molecular motor, NMII, as a novel target for chemically engineering the survival and self-renewal of hPS cells.
Actin-myosin contractility is responsible for the reduced viability of dissociated human embryonic stem cells. Cell stem cell 2010 AUG
Abstract
Human ESCs are the pluripotent precursor of the three embryonic germ layers. Human ESCs exhibit basal-apical polarity, junctional complexes, integrin-dependent matrix adhesion, and E-cadherin-dependent cell-cell adhesion, all characteristics shared by the epiblast epithelium of the intact mammalian embryo. After disruption of epithelial structures, programmed cell death is commonly observed. If individualized human ESCs are prevented from reattaching and forming colonies, their viability is significantly reduced. Here, we show that actin-myosin contraction is a critical effector of the cell death response to human ESC dissociation. Inhibition of myosin heavy chain ATPase, downregulation of myosin heavy chain, and downregulation of myosin light chain all increase survival and cloning efficiency of individualized human ESCs. ROCK inhibition decreases phosphorylation of myosin light chain, suggesting that inhibition of actin-myosin contraction is also the mechanism through which ROCK inhibitors increase cloning efficiency of human ESCs.
更多信息
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
|---|---|
| Cas Number | 856925-71-8 |
| Chemical Formula | C₁₈H₁₆N₂O₂ |
| 纯度 | ≥ 98% |
| Target | NM II ATPase |
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