EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #05702
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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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.
专为您的实验方案打造的产品
要查看实验方案所需的所有配套产品，请参阅《实验方案与技术文档》。
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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
总览
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（产品号#78003.1）和肝素溶液（产品号#07980）。
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）。
亚型
专用培养基
细胞类型
脑肿瘤干细胞，神经干/祖细胞
种属
小鼠，大鼠
应用
细胞培养，克隆筛选，扩增，功能学筛选，球状体培养，细胞毒性检测
品牌
NeuroCult
研究领域
癌症，疾病建模，神经科学，干细胞生物学
制剂类别
无血清
实验数据
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。
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 (13)
文献 (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
| 种属 | Mouse, Rat |
|---|---|
| 配方类别 | Serum-Free |
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法律声明:
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. 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.
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. 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.
