若您需要咨询产品或有任何技术问题,请通过官方电话 400 885 9050 或邮箱 info.cn@stemcell.com 与我们联系。

STEMdiff™ 神经诱导培养基

用于人 ES 和 iPS 细胞神经诱导的成分明确的无血清培养基
只有 %1
¥5,128.00

产品号 #(选择产品)

产品号 #05835_C

用于人 ES 和 iPS 细胞神经诱导的成分明确的无血清培养基

产品优势

  • 成分明确,无血清
  • 快速高效的神经诱导
  • 兼容拟胚体和单层培养方案
  • 可重复分化多种在mTeSR™ Plus、mTeSR™ 1或TeSR™-AOF中维持的ES细胞和iPS细胞系
  • 方便、便捷、用户友好的格式和操作流程

产品组分包括

  • STEMdiff™ 神经诱导培养基,250 mL(产品号 #05835)
  • STEMdiff™ 神经诱导培养基,2 x 250 mL(产品号 #05839)
Need a high-quality cell source? Use the hiPSC SCTi003-A (female) or SCTi004-A (male) control lines, manufactured with mTeSR™ Plus.

总览

STEMdiff™ 神经诱导培养基是一种成分明确的无血清培养基,用于诱导人类胚胎干细胞 (ES) 和诱导性多能干细胞 (iPS) 的神经分化。该培养基能够通过基于胚状体或单层培养的方案高效生成神经祖细胞。

您可以在我们的按需神经诱导课程中学习如何从人类多能干细胞 (hPSC) 生成神经祖细胞,并浏览我们关于使用胚状体法或单层法进行 hPSC 神经诱导的技术技巧。

分类
专用培养基
 
细胞类型
神经细胞,PSC衍生,神经干/祖细胞,多能干细胞
 
种属

 
应用
细胞培养,分化
 
品牌
STEMdiff
 
研究领域
疾病建模,神经科学,干细胞生物学
 
制剂类别
无血清
 

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。

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
05839, 05835
Lot #
All
Language
English
Document Type
Technical Manual
Catalog #
05835
Lot #
All
Language
English
Document Type
Safety Data Sheet
Catalog #
05839, 05835
Lot #
All
Language
English

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 (22)

文献 (55)

Molecular effect of ethanol during neural differentiation of human embryonic stem cells in vitro. Kim JJ et al. Genomics data 2014 DEC

Abstract

Potential teratogenic effects of alcohol on fetal development have been documented. Especially studies have demonstrated deleterious effect of ethanol exposure on neuronal development in animal models and on the maintenance and differentiation of neuronal precursor cells derived from stem cells. To better understand the molecular effect of alcohol on the process of neural differentiation,we have performed gene expression microarray analysis on human embryonic stem cells being directed to neural rosettes and neural precursor cells in the presence of ethanol treatment. Here we provide detailed experimental methods,analysis and information associated with our data deposited into Gene Expression Omnibus (GEO) under GSE56906. Our data provide scientific insight on potential molecular effects of fetal alcohol exposure on neural differentiation of early embryo development.
Multisystemic Disease Modeling of Liver-Derived Protein Folding Disorders Using Induced Pluripotent Stem Cells (iPSCs). Leung A and Murphy GJ Methods in molecular biology (Clifton,N.J.) 2016 JAN

Abstract

Familial transthyretin amyloidosis (ATTR) is an autosomal dominant protein-folding disorder caused by over 100 distinct mutations in the transthyretin (TTR) gene. In ATTR,protein secreted from the liver aggregates and forms fibrils in target organs,chiefly the heart and peripheral nervous system,highlighting the need for a model capable of recapitulating the multisystem complexity of this clinically variable disease. Here,we describe detailed methodologies for the directed differentiation of protein folding disease-specific iPSCs into hepatocytes that produce mutant protein,and neural-lineage cells often targeted in disease. Methodologies are also described for the construction of multisystem models and drug screening using iPSCs.
Genome modification leads to phenotype reversal in human myotonic dystrophy type 1 induced pluripotent stem cell-derived neural stem cells. Xia G et al. Stem cells (Dayton,Ohio) 2015 JUN

Abstract

Myotonic dystrophy type 1 (DM1) is caused by expanded CTG repeats in the 3'-untranslated region (3' UTR) of the DMPK gene. Correcting the mutation in DM1 stem cells would be an important step toward autologous stem cell therapy. The objective of this study is to demonstrate in vitro genome editing to prevent production of toxic mutant transcripts and reverse phenotypes in DM1 stem cells. Genome editing was performed in DM1 neural stem cells (NSCs) derived from human DM1 induced pluripotent stem (iPS) cells. An editing cassette containing SV40/bGH polyA signals was integrated upstream of the CTG repeats by TALEN-mediated homologous recombination (HR). The expression of mutant CUG repeats transcript was monitored by nuclear RNA foci,the molecular hallmarks of DM1,using RNA fluorescence in situ hybridization. Alternative splicing of microtubule-associated protein tau (MAPT) and muscleblind-like (MBNL) proteins were analyzed to further monitor the phenotype reversal after genome modification. The cassette was successfully inserted into DMPK intron 9 and this genomic modification led to complete disappearance of nuclear RNA foci. MAPT and MBNL 1,2 aberrant splicing in DM1 NSCs were reversed to normal pattern in genome-modified NSCs. Genome modification by integration of exogenous polyA signals upstream of the DMPK CTG repeat expansion prevents the production of toxic RNA and leads to phenotype reversal in human DM1 iPS-cells derived stem cells. Our data provide proof-of-principle evidence that genome modification may be used to generate genetically modified progenitor cells as a first step toward autologous cell transfer therapy for DM1.

更多信息

更多信息
物种
配方 无血清
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。 欲获悉更多关于STEMCELL的质控信息,请访问 STEMCELL.CN/COMPLIANCE.
Copyright © 2026 by STEMCELL Technologies. All rights reserved.

在线联系