NeuroCult™ NS-A Differentiation Kit (Human)

Medium for differentiation of human neural stem and progenitor cells

NeuroCult™ NS-A Differentiation Kit (Human)

Medium for differentiation of human neural stem and progenitor cells

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Medium for differentiation of human neural stem and progenitor cells
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What's Included

  • NeuroCult™ NS-A Basal Medium (Human), 450 mL (Catalog #05750)
  • NeuroCult™ Differentiation Supplement (Human), 50 mL

Overview

NeuroCult™ NS-A Differentiation Kit (Human) is a standardized medium for the differentiation of human neural stem and progenitor cells into neurons, astrocytes, and oligodendrocytes.
Contains
• Serum
Subtype
Specialized Media
Cell Type
Brain Tumor Stem Cells, Neural Stem and Progenitor Cells
Species
Human
Application
Cell Culture, Differentiation, Functional Assay
Brand
NeuroCult
Area of Interest
Cancer, Drug Discovery and Toxicity Testing, Neuroscience, Stem Cell Biology

Data Figures

Immunofluorescent staining to identify the differentiated cell types generated following culture of neural stem and progenitor cells in NeuroCult™ NS-A Differentiation Medium

Figure 1. Immunofluorescent Labeling to Identify the Differentiated Cell Types Generated Following Culture of Human Neural Stem and Progenitor Cells in the NeuroCult™ NS-A Differentiation Kit (Human)

A) Neurons (red) were detected with a mouse monoclonal ß-Tubulin III antibody. B) Immature oligodendrocytes (purple) were detected with a rabbit monoclonal O4 Oligodendrocyte Marker antibody. C) Astrocytes (green) were detected with a rabbit polyclonal GFAP antibody. D) Mature oligodendrocytes (purple) were detected with a galactocerebroside antibody.

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
05752
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All
Language
English
Document Type
Technical Manual
Catalog #
05752
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
05752
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
05752
Lot #
All
Language
English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Resources and Publications

Publications (13)

Humanized Stem Cell Models of Pediatric Medulloblastoma Reveal an Oct4/mTOR Axis that Promotes Malignancy M. \vCan\vcer et al. Cell Stem Cell 2019 dec

Abstract

Medulloblastoma (MB), the most frequent malignant childhood brain tumor, can arise from cellular malfunctions during hindbrain development. Here we generate humanized models for Sonic Hedgehog (SHH)-subgroup MB via MYCN overexpression in primary human hindbrain-derived neuroepithelial stem (hbNES) cells or iPSC-derived NES cells, which display a range of aggressive phenotypes upon xenografting. iPSC-derived NES tumors develop quickly with leptomeningeal dissemination, whereas hbNES-derived cells exhibit delayed tumor formation with less dissemination. Methylation and expression profiling show that tumors from both origins recapitulate hallmarks of infant SHH MB and reveal that mTOR activation, as a result of increased Oct4, promotes aggressiveness of human SHH tumors. Targeting mTOR decreases cell viability and prolongs survival, showing the utility of these varied models for dissecting mechanisms mediating tumor aggression and demonstrating the value of humanized models for a better understanding of pediatric cancers.
Cytomegalovirus infection induces a stem cell phenotype in human primary glioblastoma cells: prognostic significance and biological impact. Fornara O et al. Cell death and differentiation 2016 FEB

Abstract

Glioblastoma (GBM) is associated with poor prognosis despite aggressive surgical resection, chemotherapy, and radiation therapy. Unfortunately, this standard therapy does not target glioma cancer stem cells (GCSCs), a subpopulation of GBM cells that can give rise to recurrent tumors. GBMs express human cytomegalovirus (HCMV) proteins, and previously we found that the level of expression of HCMV immediate-early (IE) protein in GBMs is a prognostic factor for poor patient survival. In this study, we investigated the relation between HCMV infection of GBM cells and the presence of GCSCs. Primary GBMs were characterized by their expression of HCMV-IE and GCSCs marker CD133 and by patient survival. The extent to which HCMV infection of primary GBM cells induced a GCSC phenotype was evaluated in vitro. In primary GBMs, a large fraction of CD133-positive cells expressed HCMV-IE, and higher co-expression of these two proteins predicted poor patient survival. Infection of GBM cells with HCMV led to upregulation of CD133 and other GSCS markers (Notch1, Sox2, Oct4, Nestin). HCMV infection also promoted the growth of GBM cells as neurospheres, a behavior typically displayed by GCSCs, and this phenotype was prevented by either chemical inhibition of the Notch1 pathway or by treatment with the anti-viral drug ganciclovir. GBM cells that maintained expression of HCMV-IE failed to differentiate into neuronal or astrocytic phenotypes. Our findings imply that HCMV infection induces phenotypic plasticity of GBM cells to promote GCSC features and may thereby increase the aggressiveness of this tumor.
Rapid and Efficient Direct Conversion of Human Adult Somatic Cells into Neural Stem Cells by HMGA2/let-7b. Yu K-R et al. Cell reports 2015 JAN

Abstract

A recent study has suggested that fibroblasts can be converted into mouse-induced neural stem cells (miNSCs) through the expression of defined factors. However, successful generation of human iNSCs (hiNSCs) has proven challenging to achieve. Here, using microRNA (miRNA) expression profile analyses, we showed that let-7 microRNA has critical roles for the formation of PAX6/NESTIN-positive colonies from human adult fibroblasts and the proliferation and self-renewal of hiNSCs. HMGA2, a let-7-targeting gene, enables induction of hiNSCs that displayed morphological/molecular features and in vitro/in vivo differentiation potential similar to H9-derived NSCs. Interestingly, HMGA2 facilitated the efficient conversion of senescent somatic cells or blood CD34+ cells into hiNSCs through an interaction with SOX2, whereas other combinations or SOX2 alone showed a limited conversion ability. Taken together, these findings suggest that HMGA2/let-7 facilitates direct reprogramming toward hiNSCs in minimal conditions and maintains hiNSC self-renewal, providing a strategy for the clinical treatment of neurological diseases.