EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72252_C
RHO/ROCK 通路抑制剂；抑制 ROCK
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总览
Thiazovivin 是 Rho 相关卷曲螺旋蛋白激酶 (ROCK) 的选择性抑制剂，ROCK 是一种丝氨酸/苏氨酸激酶，在细胞极性、收缩和肌动蛋白细胞骨架重组中发挥作用 (Xu et al.)。Thiazovivin 的有效浓度比另一种常见的 ROCK 抑制剂 Y-27632（产品号 #72302；Xu et al.）低 5 倍。
维持和自我更新
·通通过稳定 E-钙粘蛋白促进人胚胎干细胞 (ES) 在分离过程中的存活，并改善细胞附着（Xu et al.）。
·在转染 TALEN 介导的基因组编辑过程中促进单个人诱导多能干细胞 (iPS) 的存活（Sun and Zhao）。
重编程
·与 PD0325091 和 SB431542 结合使用，可提高将人体细胞重新编程为 iPS 细胞的效率（Lin et al.）。
·提高将人脐带血单核细胞重新编程为 iPS 细胞的效率（Hu et al.）。
细胞类型
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，重编程
研究领域
细胞系制备，干细胞生物学
CAS 编号
1226056-71-8
化学式
C₁₅H₁₃N₅OS
纯度
≥98%
通路
RHO/ROCK
靶点
ROCK
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 (4)
Seamless correction of the sickle cell disease mutation of the HBB gene in human induced pluripotent stem cells using TALENs. Biotechnology and Bioengineering 2014 MAY
Abstract
Sickle cell disease (SCD) is the most common human genetic disease which is caused by a single mutation of human β-globin (HBB) gene. The lack of long-term treatment makes the development of reliable cell and gene therapies highly desirable. Disease-specific patient-derived human induced pluripotent stem cells (hiPSCs) have great potential for developing novel cell and gene therapies. With the disease-causing mutations corrected in situ, patient-derived hiPSCs can restore normal cell functions and serve as a renewable autologous cell source for the treatment of genetic disorders. Here we successfully utilized transcription activator-like effector nucleases (TALENs), a recently emerged novel genome editing tool, to correct the SCD mutation in patient-derived hiPSCs. The TALENs we have engineered are highly specific and generate minimal off-target effects. In combination with piggyBac transposon, TALEN-mediated gene targeting leaves no residual ectopic sequences at the site of correction and the corrected hiPSCs retain full pluripotency and a normal karyotype. Our study demonstrates an important first step of using TALENs for the treatment of genetic diseases such as SCD, which represents a significant advance toward hiPSC-based cell and gene therapies.
Efficient generation of transgene-free induced pluripotent stem cells from normal and neoplastic bone marrow and cord blood mononuclear cells. Blood 2011 APR
Abstract
Reprogramming blood cells to induced pluripotent stem cells (iPSCs) provides a novel tool for modeling blood diseases in vitro. However, the well-known limitations of current reprogramming technologies include low efficiency, slow kinetics, and transgene integration and residual expression. In the present study, we have demonstrated that iPSCs free of transgene and vector sequences could be generated from human BM and CB mononuclear cells using non-integrating episomal vectors. The reprogramming described here is up to 100 times more efficient, occurs 1-3 weeks faster compared with the reprogramming of fibroblasts, and does not require isolation of progenitors or multiple rounds of transfection. Blood-derived iPSC lines lacked rearrangements of IGH and TCR, indicating that their origin is non-B- or non-T-lymphoid cells. When cocultured on OP9, blood-derived iPSCs could be differentiated back to the blood cells, albeit with lower efficiency compared to fibroblast-derived iPSCs. We also generated transgene-free iPSCs from the BM of a patient with chronic myeloid leukemia (CML). CML iPSCs showed a unique complex chromosomal translocation identified in marrow sample while displaying typical embryonic stem cell phenotype and pluripotent differentiation potential. This approach provides an opportunity to explore banked normal and diseased CB and BM samples without the limitations associated with virus-based methods.
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.
更多信息
| 种属 | Human, Mouse, Non-Human Primate, Other, Rat |
|---|---|
| Cas Number | 1226056-71-8 |
| Chemical Formula | C₁₅H₁₃N₅OS |
| 纯度 | ≥ 98% |
| Target | ROCK |
| Pathway | RHO/ROCK |
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