NeuroCult™ Proliferation Kit (Mouse & Rat)

Medium kit for expansion of mouse and rat neural stem and progenitor cells

You may notice that your reagent packaging looks slightly different from images displayed here or from previous orders. Due to pandemic-related plasticware shortages, we are temporarily using alternative bottles for this product. Rest assured that the products themselves and how you should use them have not changed.

NeuroCult™ Proliferation Kit (Mouse & Rat)

Medium kit for expansion of mouse and rat neural stem and progenitor cells

NeuroCult™ Proliferation Kit (Mouse & Rat)
1 Kit
250 USD
Catalog # 05702

Medium kit for expansion of mouse and rat neural stem and progenitor cells

What's Included

  • NeuroCult™ Basal Medium (Mouse & Rat), 450 mL
  • NeuroCult™ Proliferation Supplement (Mouse & Rat), 50 mL
You may notice that your reagent packaging looks slightly different from images displayed here or from previous orders. Due to pandemic-related plasticware shortages, we are temporarily using alternative bottles for this product. Rest assured that the products themselves and how you should use them have not changed.
Products for Your Protocol
To see all required products for your protocol, please consult the Protocols and Documentation.

Overview

NeuroCult™ Proliferation Kit (Mouse & Rat) is a standardized, serum-free medium and supplement kit for the culture of mouse and rat neural stem and progenitor cells from normal tissues or tumor samples. When supplemented with appropriate cytokines, NeuroCult™ Proliferation Kit (Mouse & Rat) is optimized to maintain mouse and rat neural stem cells in culture for extended periods of time without the loss of their self-renewal, proliferation, or differentiation potential.

NOTE: When preparing Complete NeuroCult™ Proliferation Medium, addition of Human Recombinant EGF (Catalog #78006.1) is required. When culturing cells obtained from adult mouse or rat, Human Recombinant bFGF (Catalog #78003.1) and Heparin Solution (Catalog #07980) are also required.
Subtype
Specialized Media
Cell Type
Brain Tumor Stem Cells, Neural Stem and Progenitor Cells
Species
Mouse, Rat
Application
Cell Culture, Colony Assay, Expansion, Functional Assay, Spheroid Culture, Toxicity Assay
Brand
NeuroCult
Area of Interest
Cancer, Disease Modeling, Neuroscience, Stem Cell Biology
Formulation
Serum-Free

Data Figures

Figure 1. Comparison of Cell Expansion for Mouse Neurospheres Cultured with Complete NeuroCult™ Proliferation Medium (Mouse & Rat) or a Traditional Formulation

Cells microdissected from the cortices of E14 mice were cultured in Complete NeuroCult™ Proliferation Medium (Mouse & Rat) or a traditional formulation containing 20 ng/mL rh EGF. At Day 71, cells cultured in Complete NeuroCult™ Proliferation Medium (Mouse & Rat) were at Passage 13 while cells cultured in a traditional medium formulation were at Passage 10. Complete NeuroCult™ Proliferation Medium (Mouse & Rat) consists of NeuroCult™ NSC Basal Medium (Mouse & Rat), NeuroCult™ NSC Proliferation Supplement (Mouse & Rat) and 20 ng/mL rh EGF.

Figure 2. Cell Expansion for Rat Neurospheres Cultured with Complete NeuroCult™ Proliferation Medium (Mouse & Rat)

Cells microdissected from the cortices of E18 rat were cultured in 3 different lots of NeuroCult™ Proliferation Medium (Mouse & Rat). In each sample, cells continued to generate neurospheres beyond passage 5, resulting in an increase in total cell number. At passages 1 and 5, cells dissociated from the neurospheres were able to differentiate into neurons, oligodendrocytes and astrocytes [data not shown].

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 #
05702
Lot #
All
Language
English
Catalog #
05702
Lot #
All
Language
English
Document Type
Technical Manual
Catalog #
05702
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
05702
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
05702
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 (113)

Recombinant insulin-like growth factor binding protein-4 inhibits proliferation and promotes differentiation of neural progenitor cells Niu H et al. Neuroscience Letters 2017 MAR

Abstract

Insulin-like growth factor (IGF) is involved in regulating many processes during neural development, and IGF binding protein-4 (IGFBP4) functions as a modulator of IGF actions or in an IGF-independent manner (e.g., via inhibiting Wnt/β-catenin signaling). In the present study, neural progenitor cells (NPCs) were isolated from the forebrain of newborn mice to investigate effects of IGFBP4 on the proliferation and differentiation of NPCs. The proliferation of NPCs was evaluated using Cell Counting Kit-8 (CCK-8) after treatment with or without IGFBP4 as well as blockers of IGF-IR and β-catenin. Phosphorylation levels of Akt, Erk1, 2 and p38 were analyzed by Western blotting. The differentiation of NPCs was evaluated using immunofluorescence and Western blotting. It was shown that exogenous IGFBP4 significantly inhibited the proliferation of NPCs and it did not induce a more pronounced inhibition of cell proliferation after blockade of IGF-IR but it did after antagonism of β-catenin. Akt phosphorylation was significantly decreased and phosphorylation levels of Erk1, 2 and p38 were not significantly changed in IGFBP4-treated NPCs. Excessive IGFBP4 significantly promoted NPCs to differentiate into astrocytes and neurons. These data suggested that exogenous IGFBP4 inhibits proliferation and promotes differentiation of neural progenitor cells mainly through IGF-IR signaling pathway.
Cathepsin B Improves ß-Amyloidosis and Learning and Memory in Models of Alzheimer's Disease. Embury CM et al. Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology 2017 JUN

Abstract

Amyloid-ß (Aß) precursor protein (APP) metabolism engages neuronal endolysosomal pathways for Aß processing and secretion. In Alzheimer's disease (AD), dysregulation of APP leads to excess Aß and neuronal dysfunction; suggesting that neuronal APP/Aß trafficking can be targeted for therapeutic gain. Cathepsin B (CatB) is a lysosomal cysteine protease that can lower Aß levels. However, whether CatB-modulation of Aß improves learning and memory function deficits in AD is not known. To this end, progenitor neurons were infected with recombinant adenovirus expressing CatB and recovered cell lysates subjected to proteomic analyses. The results demonstrated Lamp1 deregulation and linkages between CatB and the neuronal phagosome network. Hippocampal injections of adeno-associated virus expressing CatB reduced Aß levels, increased Lamp1 and improved learning and memory. The findings were associated with the emergence of c-fos + cells. The results support the idea that CatB can speed Aß metabolism through lysosomal pathways and as such reduce AD-associated memory deficits.
Qki deficiency maintains stemness of glioma stem cells in suboptimal environment by downregulating endolysosomal degradation. Shingu T et al. Nature genetics 2017 JAN

Abstract

Stem cells, including cancer stem cells (CSCs), require niches to maintain stemness, yet it is unclear how CSCs maintain stemness in the suboptimal environment outside their niches during invasion. Postnatal co-deletion of Pten and Trp53 in mouse neural stem cells (NSCs) leads to the expansion of these cells in their subventricular zone (SVZ) niches but fails to maintain stemness outside the SVZ. We discovered that Qki is a major regulator of NSC stemness. Qk deletion on a Pten-/-; Trp53-/- background helps NSCs maintain their stemness outside the SVZ in Nes-CreERT2; QkL/L; PtenL/L; Trp53L/L mice, which develop glioblastoma with a penetrance of 92% and a median survival time of 105 d. Mechanistically, Qk deletion decreases endolysosome-mediated degradation and enriches receptors essential for maintaining self-renewal on the cytoplasmic membrane to cope with low ligand levels outside niches. Thus, downregulation of endolysosome levels by Qki loss helps glioma stem cells (GSCs) maintain their stemness in suboptimal environments outside their niches.

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