产品号 #05702_C
小鼠和大鼠神经干细胞及祖细胞扩增培养基套装
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Products for Your Protocol
To see all required products for your protocol, please consult the Protocols and Documentation.
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Heparin SolutionCell culture supplement
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Human Recombinant bFGFBasic fibroblast growth factor
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Human Recombinant EGFEpidermal growth factor
概述
NeuroCult™增殖套装（小鼠和大鼠）是一种标准化的无血清培养基及添加剂套装，用于培养来自正常组织或肿瘤样本的小鼠和大鼠神经干细胞及祖细胞。在添加适当细胞因子后，NeuroCult™扩增套装（小鼠和大鼠）经过优化，可长时间维持培养小鼠和大鼠神经干细胞，且不会丧失其自我更新、扩增或分化潜能。
注意：配制NeuroCult™完全扩增培养基时，需添加人重组EGF（产品编号#78006.1）。培养来自成年小鼠或大鼠的细胞时，还需添加人重组bFGF（产品编号#78003.1）和肝素溶液（产品编号#07980）。
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 Category
Serum-Free
Data Figures
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
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
Educational Materials (13)
Publications (113)
Recombinant insulin-like growth factor binding protein-4 inhibits proliferation and promotes differentiation of neural progenitor cells 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. 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. 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.
更多信息
| Species | Mouse, Rat |
|---|---|
| Formulation Category | Serum-Free |
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Legal Statement: Sold under license from StemCells California, Inc. US Patent Nos. 5,750,376; 5,851,832; 5,980,885; 5,968,829; 5,981,165; 6,071,889; 6,093,531; 6,103,530; 6,165,783; 6,238,922. PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT STEMCELL, REFER TO WWW.STEMCELL.COM/COMPLIANCE.
