EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #05270_C
用于将人ES和iPS细胞分化为多种谱系的成分明确的无动物源培养基
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总览
STEMdiff™ APEL™ 2 培养基是一种成分明确、无血清、无动物源的培养基，用于人胚胎干细胞 (ES) 和诱导多能干细胞 (iPS)的分化。该培养基基于 Andrew Elefanty 博士发表的 APEL 配方，不含任何诸如无蛋白杂交瘤培养基等不明确的成分。STEMdiff™ APEL™ 2 可用于贴壁或拟胚体 (EB) 的分化方案，例如与 AggreWell™ 配合使用。该培养基可以搭配多种不同的诱导因子或细胞因子使用，以支持向外胚层、中胚层和内胚层谱系的分化。
分类
专用培养基
细胞类型
多能干细胞
种属
人
应用
细胞培养，分化
品牌
STEMdiff
研究领域
干细胞生物学
制剂类别
无动物源
实验数据
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 (5)
文献 (22)
Efficient derivation of lateral plate and paraxial mesoderm subtypes from human embryonic stem cells through GSKi-mediated differentiation.
Stem cells and development 2013 JUL
Abstract
The vertebrae mesoderm is a source of cells that forms a variety of tissues,including the heart,vasculature,and blood. Consequently,the derivation of various mesoderm-specific cell types from human embryonic stem cells (hESCs) has attracted the interest of many investigators owing to their therapeutic potential in clinical applications. However,the need for efficient and reliable methods of differentiation into mesoderm lineage cell types remains a significant challenge. Here,we demonstrated that inhibition of glycogen synthase kinase-3 (GSK-3) is an essential first step toward efficient generation of the mesoderm. Under chemically defined conditions without additional growth factors/cytokines,short-term GSK inhibitor (GSKi) treatment effectively drives differentiation of hESCs into the primitive streak (PS),which can potentially commit toward the mesoderm when further supplemented with bone morphogenetic protein 4. Further analysis confirmed that the PS-like cells derived from GSKi treatment are bipotential,being able to specify toward the endoderm as well. Our findings suggest that the bipotential,PS/mesendoderm-like cell population exists only at the initial stages of GSK-3 inhibition,whereas long-term inhibition results in an endodermal fate. Lastly,we demonstrated that our differentiation approach could efficiently generate lateral plate (CD34(+)KDR(+)) and paraxial (CD34(-)PDGFRα(+)) mesoderm subsets that can be further differentiated along the endothelial and smooth muscle lineages,respectively. In conclusion,our study presents a unique approach for generating early mesoderm progenitors in a chemically directed fashion through the use of small-molecule GSK-3 inhibitor,which may be useful for future applications in regenerative medicine.
The epigenetic modifier ubiquitin-specific protease 22 (USP22) regulates embryonic stem cell differentiation via transcriptional repression of sex-determining region Y-box 2 (SOX2)
Journal of Biological Chemistry 2013 AUG
Abstract
Pluripotent embryonic stem cells (ESCs) undergo self-renewal until stimulated to differentiate along specific lineage pathways. Many of the transcriptional networks that drive reprogramming of a self-renewing ESC to a differentiating cell have been identified. However,fundamental questions remain unanswered about the epigenetic programs that control these changes in gene expression. Here we report that the histone ubiquitin hydrolase ubiquitin-specific protease 22 (USP22) is a critical epigenetic modifier that controls this transition from self-renewal to differentiation. USP22 is induced as ESCs differentiate and is necessary for differentiation into all three germ layers. We further report that USP22 is a transcriptional repressor of the locus encoding the core pluripotency factor sex-determining region Y-box 2 (SOX2) in ESCs,and this repression is required for efficient differentiation. USP22 occupies the Sox2 promoter and hydrolyzes monoubiquitin from ubiquitylated histone H2B and blocks transcription of the Sox2 locus. Our study reveals an epigenetic mechanism that represses the core pluripotency transcriptional network in ESCs,allowing ESCs to transition from a state of self-renewal into lineage-specific differentiation programs.
Erythropoietin critically regulates the terminal maturation of murine and human primitive erythroblasts
Haematologica 2013 NOV
Abstract
Primitive erythroid cells,the first red blood cells produced in the mammalian embryo,are necessary for embryonic survival. Erythropoietin and its receptor EpoR,are absolutely required for survival of late-stage definitive erythroid progenitors in the fetal liver and adult bone marrow. Epo- and Epor-null mice die at E13.5 with a lack of definitive erythrocytes. However,the persistence of circulating primitive erythroblasts raises questions about the role of erythropoietin/EpoR in primitive erythropoiesis. Using Epor-null mice and a novel primitive erythroid 2-step culture we found that erythropoietin is not necessary for specification of primitive erythroid progenitors. However,Epor-null embryos develop a progressive,profound anemia by E12.5 as primitive erythroblasts mature as a synchronous cohort. This anemia results from reduced primitive erythroblast proliferation associated with increased p27 expression,from advanced cellular maturation,and from markedly elevated rates of apoptosis associated with an imbalance in pro- and anti-apoptotic gene expression. Both mouse and human primitive erythroblasts cultured without erythropoietin also undergo accelerated maturation and apoptosis at later stages of maturation. We conclude that erythropoietin plays an evolutionarily conserved role in promoting the proliferation,survival,and appropriate timing of terminal maturation of primitive erythroid precursors.
更多信息
| 物种 | 人 |
|---|---|
| 配方 | 无动物源性 |
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