NeuroCult™ NS-A Basal Medium (Human)

Basal medium for expansion of human neural stem and progenitor cells
NeuroCult™ NS-A Basal Medium (Human)

Basal medium for expansion of human neural stem and progenitor cells

450 mL
Catalog # 05750
92 USD
Required Products
  1. Heparin Solution
    Heparin Solution

    Cell culture supplement

  2. Human Recombinant bFGF
    Human Recombinant bFGF

    Basic fibroblast growth factor

  3. Human Recombinant EGF
    Human Recombinant EGF

    Epidermal growth factor

Overview

NeuroCult™ NS-A Basal Medium (Human) is a standardized basal medium for the expansion of human neural stem cells and brain tumor stem cells, in the neurosphere or adherent monolayer culture system. This basal medium is a component of the NeuroCult™ NS-A Proliferation Kit (Human; Catalog #05751) and the NeuroCult™ NS-A Differentiation Kit (Human; Catalog #05752).
Subtype
Basal Media, Specialized Media
Cell Type
Brain Tumor Stem Cells, Neural Stem and Progenitor Cells
Species
Human
Application
Cell Culture, Colony Assay, Differentiation, Expansion, Functional Assay, Spheroid Culture
Brand
NeuroCult
Area of Interest
Cancer, Drug Discovery and Toxicity Testing, Neuroscience, Stem Cell Biology
Formulation
Serum-Free

Scientific Resources

Product Documentation

Document Type Product Name Catalog # Lot # Language
Document Type
Product Information Sheet
Product Name
NeuroCult™ NS-A Basal Medium (Human)
Catalog #
05750
Lot #
All
Language
English
Document Type
Safety Data Sheet
Product Name
NeuroCult™ NS-A Basal Medium (Human)
Catalog #
05750
Lot #
All
Language
English

Educational Materials (8)

Brochure
STEMCELL Neural Product Portfolio
Protocol
How to Cryopreserve Neurospheres
Wallchart
Neural Stem Cells
Wallchart
SnapShot: Glioblastoma Multiforme
Webinar
Standardized Media and Reagents for Neural Stem Cell Research with NeuroCult™
41:19
Standardized Media and Reagents for Neural Stem Cell Research with NeuroCult™
Webinar
Neural Stem Cell Culture Systems - Neurosphere vs. Adherent Monolayer Culture
47:21
Neural Stem Cell Culture Systems - Neurosphere vs. Adherent Monolayer Culture
Webinar
Identification and Characterization of Neural Stem Cells: Why is This so Darned Difficult?
1:06:37
Identification and Characterization of Neural Stem Cells: Why is This so Darned Difficult?
Mini Review
Neural Stem Cells: Identification, Function, Culture, and Isolation

Product 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.

Data and Publications

Publications (98)

Viruses 2020 mar Modelling Lyssavirus Infections in Human Stem Cell-Derived Neural Cultures. V. Sundaramoorthy et al.

Abstract

Rabies is a zoonotic neurological infection caused by lyssavirus that continues to result in devastating loss of human life. Many aspects of rabies pathogenesis in human neurons are not well understood. Lack of appropriate ex-vivo models for studying rabies infection in human neurons has contributed to this knowledge gap. In this study, we utilize advances in stem cell technology to characterize rabies infection in human stem cell-derived neurons. We show key cellular features of rabies infection in our human neural cultures, including upregulation of inflammatory chemokines, lack of neuronal apoptosis, and axonal transmission of viruses in neuronal networks. In addition, we highlight specific differences in cellular pathogenesis between laboratory-adapted and field strain lyssavirus. This study therefore defines the first stem cell-derived ex-vivo model system to study rabies pathogenesis in human neurons. This new model system demonstrates the potential for enabling an increased understanding of molecular mechanisms in human rabies, which could lead to improved control methods.
Nature communications 2020 jul Single-cell RNA-seq reveals that glioblastoma recapitulates a normal neurodevelopmental hierarchy. C. P. Couturier et al.

Abstract

Cancer stem cells are critical for cancer initiation, development, and treatment resistance. Our understanding of these processes, and how they relate to glioblastoma heterogeneity, is limited. To overcome these limitations, we performed single-cell RNA sequencing on 53586 adult glioblastoma cells and 22637 normal human fetal brain cells, and compared the lineage hierarchy of the developing human brain to the transcriptome of cancer cells. We find a conserved neural tri-lineage cancer hierarchy centered around glial progenitor-like cells. We also find that this progenitor population contains the majority of the cancer's cycling cells, and, using RNA velocity, is often the originator of the other cell types. Finally, we show that this hierarchal map can be used to identify therapeutic targets specific to progenitor cancer stem cells. Our analyses show that normal brain development reconciles glioblastoma development, suggests a possible origin for glioblastoma hierarchy, and helps to identify cancer stem cell-specific targets.
Scientific reports 2019 nov Higher Order Architecture of Designer Peptides Forms Bioinspired 10 nm siRNA Delivery System. A. Gamboa et al.

Abstract

The higher-order architecture observed in biological systems, like viruses, is very effective in nucleic acid transport. The replications of this system has been attempted with both synthetic and naturally occurring polymers with mixed results. Here we describe a peptide/siRNA quaternary complex that functions as an siRNA delivery system. The rational design of a peptide assembly is inspired by the viral capsids, but not derived from them. We selected the collagen peptide (COL) to provide the structural stability and the folding framework, and hybridize it with the cell penetrating peptide (CPP) that allows for effective penetration of biological barriers. The peptide/siRNA quaternary complex forms stoichiometric, 10 nm nanoparticles, that show fast cellular uptake ({\textless}30 min), effective siRNA release, and gene silencing. The complex provides capsid-like protection for siRNA against nucleases without being immunostimulatory, or cytotoxic. Our data suggests that delivery vehicles based on synthetic quaternary structures that exhibit higher-order architecture may be effective in improving delivery and release of nucleic acid cargo.
Scientific Reports 2019 dec BMP signaling mediates glioma stem cell quiescence and confers treatment resistance in glioblastoma R. Sachdeva et al.

Abstract

Despite advances in therapy, glioblastoma remains an incurable disease with a dismal prognosis. Recent studies have implicated cancer stem cells within glioblastoma (glioma stem cells, GSCs) as mediators of therapeutic resistance and tumor progression. In this study, we investigated the role of the transforming growth factor-$\beta$ (TGF-$\beta$) superfamily, which has been found to play an integral role in the maintenance of stem cell homeostasis within multiple stem cell systems, as a mediator of stem-like cells in glioblastoma. We find that BMP and TGF-$\beta$ signaling define divergent molecular and functional identities in glioblastoma, and mark relatively quiescent and proliferative GSCs, respectively. Treatment of GSCs with BMP inhibits cell proliferation, but does not abrogate their stem-ness, as measured by self-renewal and tumorigencity. Further, BMP pathway activation confers relative resistance to radiation and temozolomide chemotherapy. Our findings define a quiescent cancer stem cell population in glioblastoma that may be a cellular reservoir for tumor recurrence following cytotoxic therapy.
Nature communications 2019 G-quadruplex DNA drives genomic instability and represents a targetable molecular abnormality in ATRX-deficient malignant glioma. Y. Wang et al.

Abstract

Mutational inactivation of ATRX ($\alpha$-thalassemia mental retardation X-linked) represents a defining molecular alteration in large subsets of malignant glioma. Yet the pathogenic consequences of ATRX deficiency remain unclear, as do tractable mechanisms for its therapeutic targeting. Here we report that ATRX loss in isogenic glioma model systems induces replication stress and DNA damage by way of G-quadruplex (G4) DNA secondary structure. Moreover, these effects are associated with the acquisition of disease-relevant copy number alterations over time. We then demonstrate, both in vitro and in vivo, that ATRX deficiency selectively enhances DNA damage and cell death following chemical G4 stabilization. Finally, we show that G4 stabilization synergizes with other DNA-damaging therapies, including ionizing radiation, in the ATRX-deficient context. Our findings reveal novel pathogenic mechanisms driven by ATRX deficiency in glioma, while also pointing to tangible strategies for drug development.
Clinical cancer research : an official journal of the American Association for Cancer Research 2019 Mechanisms and Antitumor Activity of a Binary EGFR/DNA-Targeting Strategy Overcomes Resistance of Glioblastoma Stem Cells to Temozolomide. Z. Sharifi et al.

Abstract

PURPOSE Glioblastoma (GBM) is a fatal primary malignant brain tumor. GBM stem cells (GSC) contribute to resistance to the DNA-damaging chemotherapy, temozolomide. The epidermal growth factor receptor (EGFR) displays genomic alterations enabling DNA repair mechanisms in half of GBMs. We aimed to investigate EGFR/DNA combi-targeting in GBM. EXPERIMENTAL DESIGN ZR2002 is a combi-molecule" designed to inflict DNA damage through its chlorethyl moiety and induce irreversible EGFR tyrosine kinase inhibition. We assessed its in vitro efficacy in temozolomide-resistant patient-derived GSCs mesenchymal temozolomide-sensitive and resistant in vivo-derived GSC sublines and U87/EGFR isogenic cell lines stably expressing EGFR/wild-type or variant III (EGFRvIII). We evaluated its antitumor activity in mice harboring orthotopic EGFRvIII or mesenchymal TMZ-resistant GSC tumors. RESULTS ZR2002 induced submicromolar antiproliferative effects and inhibited neurosphere formation of all GSCs with marginal effects on normal human astrocytes. ZR2002 inhibited EGF-induced autophosphorylation of EGFR downstream Erk1/2 phosphorylation increased DNA strand breaks and induced activation of wild-type p53; the latter was required for its cytotoxicity through p53-dependent mechanism. ZR2002 induced similar effects on U87/EGFR cell lines and its oral administration significantly increased survival in an orthotopic EGFRvIII mouse model. ZR2002 improved survival of mice harboring intracranial mesenchymal temozolomide-resistant GSC line decreased EGFR Erk1/2 and AKT phosphorylation and was detected in tumor brain tissue by MALDI imaging mass spectrometry. CONCLUSIONS These findings provide the molecular basis of binary EGFR/DNA targeting and uncover the oral bioavailability blood-brain barrier permeability and antitumor activity of ZR2002 supporting potential evaluation of this first-in-class drug in recurrent GBM."
View All Publications

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