EpiCult™-B Mouse Mammary Epithelial Cell Medium Kit

总览

EpiCult™-B（小鼠）是一种无血清液体培养基，专为培养小鼠乳腺腔细胞和肌上皮细胞而优化。它与辐照饲养层细胞（例如NIH 3T3细胞）配合使用，是乳腺集落形成单位（CMD）实验中培养和评估小鼠乳腺上皮祖细胞的理想选择。添加胶原酶和透明质酸酶后，该培养基也可用于小鼠乳腺组织的酶解。培养细胞时需要添加人重组EGF（产品号 #78006）、人重组bFGF（产品号 #78003）和肝素溶液（产品号 #07980）。

亚型
专用培养基

细胞类型
乳腺细胞

种属
小鼠

应用
细胞培养，克隆筛选

品牌
EpiCult

研究领域
上皮细胞研究

制剂类别
无血清

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实验数据

Figure 1. Protocol for Isolation and Identification of Human and Mouse Mammary Epithelial Progenitor Cells

Phase contrast photographs of (A) a pure human myoepithelial cell colony, (B) a pure human luminal cell colony, and (C) a mixed human colony. (D) is a mouse colony. Unlike human mammary CFC colonies, subtypes of mouse mammary epithelial cell colonies are not easily identifiable. All colonies were cultured in either EpiCult®-B (Human: Catalog #05601) or EpiCult®-B (Mouse:Catalog #5610) in the presence of an irradiated NIH 3T3 feeder layer. Colonies were visualized by staining with Wright"s Giemsa. (E) is a picture of mammospheres obtained from primary human mammary epithelial cells and (F) is an image of tumorspheres obtained from MCF7 human breast cancer cell line.

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。

Document Type

Product Name

Catalog #

Lot #

Language

Document Type

Product Information Sheet

Product Name

EpiCult™-B Mouse Medium Kit

Catalog #

05610

Lot #

All

Language

English

Document Type

Safety Data Sheet 1

Product Name

EpiCult™-B Mouse Medium Kit

Catalog #

05610

Lot #

All

Language

English

Document Type

Safety Data Sheet 2

Product Name

EpiCult™-B Mouse Medium Kit

Catalog #

05610

Lot #

All

Language

English

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。

Research Area

Workflow Stages

Workflow Stages for Mammary Epithelial Cell Research

Tissue Dissociation and Isolation

Cell Culture and Assay

Characterization

相关材料与文献

Sterol regulatory element binding protein 1 couples mechanical cues and lipid metabolism. R. Bertolio et al. Nature communications 2019

Abstract

Sterol regulatory element binding proteins (SREBPs) are a family of transcription factors that regulate lipid biosynthesis and adipogenesis by controlling the expression of several enzymes required for cholesterol, fatty acid, triacylglycerol and phospholipid synthesis. In vertebrates, SREBP activation is mainly controlled by a complex and well-characterized feedback mechanism mediated by cholesterol, a crucial bio-product of the SREBP-activated mevalonate pathway. In this work, we identified acto-myosin contractility and mechanical forces imposed by the extracellular matrix (ECM) as SREBP1 regulators. SREBP1 control by mechanical cues depends on geranylgeranyl pyrophosphate, another key bio-product of the mevalonate pathway, and impacts on stem cell fate in mouse and on fat storage in Drosophila. Mechanistically, we show that activation of AMP-activated protein kinase (AMPK) by ECM stiffening and geranylgeranylated RhoA-dependent acto-myosin contraction inhibits SREBP1 activation. Our results unveil an unpredicted and evolutionary conserved role of SREBP1 in rewiring cell metabolism in response to mechanical cues.

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Development of mammary luminal progenitor cells is controlled by the transcription factor STAT5A. Yamaji D et al. Genes & development 2009 OCT

Abstract

Mammary alveologenesis is abrogated in the absence of the transcription factors STAT5A/5B, which mediate cytokine signaling. To reveal the underlying causes for this developmental block, we studied mammary stem and progenitor cells. While loss of STAT5A/5B did not affect the stem cell population and its ability to form mammary ducts, luminal progenitors were greatly reduced and unable to form alveoli during pregnancy. Temporally controlled expression of transgenic STAT5A in mammary epithelium lacking STAT5A/5B restored the luminal progenitor population and rescued alveologenesis in a reversible fashion in vivo. Thus, STAT5A is necessary and sufficient for the establishment of luminal progenitor cells.

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MMTV-Wnt1 and -DeltaN89beta-catenin induce canonical signaling in distinct progenitors and differentially activate Hedgehog signaling within mammary tumors. Teissedre B et al. PloS one 2009 JAN

Abstract

Canonical Wnt/beta-catenin signaling regulates stem/progenitor cells and, when perturbed, induces many human cancers. A significant proportion of human breast cancer is associated with loss of secreted Wnt antagonists and mice expressing MMTV-Wnt1 and MMTV-DeltaN89beta-catenin develop mammary adenocarcinomas. Many studies have assumed these mouse models of breast cancer to be equivalent. Here we show that MMTV-Wnt1 and MMTV-DeltaN89beta-catenin transgenes induce tumors with different phenotypes. Using axin2/conductin reporter genes we show that MMTV-Wnt1 and MMTV-DeltaN89beta-catenin activate canonical Wnt signaling within distinct cell-types. DeltaN89beta-catenin activated signaling within a luminal subpopulation scattered along ducts that exhibited a K18(+)ER(-)PR(-)CD24(high)CD49f(low) profile and progenitor properties. In contrast, MMTV-Wnt1 induced canonical signaling in K14(+) basal cells with CD24/CD49f profiles characteristic of two distinct stem/progenitor cell-types. MMTV-Wnt1 produced additional profound effects on multiple cell-types that correlated with focal activation of the Hedgehog pathway. We document that large melanocytic nevi are a hitherto unreported hallmark of early hyperplastic Wnt1 glands. These nevi formed along the primary mammary ducts and were associated with Hedgehog pathway activity within a subset of melanocytes and surrounding stroma. Hh pathway activity also occurred within tumor-associated stromal and K14(+)/p63(+) subpopulations in a manner correlated with Wnt1 tumor onset. These data show MMTV-Wnt1 and MMTV-DeltaN89beta-catenin induce canonical signaling in distinct progenitors and that Hedgehog pathway activation is linked to melanocytic nevi and mammary tumor onset arising from excess Wnt1 ligand. They further suggest that Hedgehog pathway activation maybe a critical component and useful indicator of breast tumors arising from unopposed Wnt1 ligand.

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