EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #06010_C
用于建立和维持人肠道类器官的培养基
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Interested in trying STEMCELL’s organoid products for your intestinal research? Fill out the form to request information about introductory offers.
What Our Scientist Says
Organoids have truly expanded the limits of what's possible for in vitro studies of the intestinal epithelium. By providing optimized culture media and robust, approachable protocols, we are making these technologies more accessible to researchers.
Ryan ConderAssociate Director, Gastrointestinal Biology
总览
使用该完整培养基配方和优化的实验方案，构建和维持肠道类器官，以模拟成年肠上皮的关键特性。凭借该易于操作且有效的实验流程，可在一周内自人体肠隐窝衍生出类器官；富集的干细胞群促进了不同供体来源的类器官的生长，即使是原本较难培养的供体样本也能获得良好结果。
在IntestiCult™ 类器官生长培养基 (人)中生长的类器官包含一个由具有极性的肠上皮细胞层包围而成的功能性腔体结构。为满足多样化的建模应用，这些类器官可在三维结构中，或在浸没式单层培养或气液界面（ALI）培养的二维结构中，通过 IntestiCult™ 类器官分化培养基（人）（产品号 #100-0214）实现进一步分化。
肠类器官培养的应用包括研究肠道上皮的发育和功能、构建肠道疾病模型，以及在肠道模型中筛选分子的有效性和毒性。肠类器官培养还可用于研究成体干细胞特性及再生治疗方法。
欢迎通过我们的免费点播课程学习人肠类器官的培养方法，或浏览关于使用 IntestiCult™ 进行类器官培养流程的常见问题（FAQs）。此外，您还可以下载我们的电子书《肠道类器官培养方案：入门指南及进阶方案》，获取肠类器官培养方案的精选合集。
如果您打算将本产品用于商业目的，请通过www.huborganoids.nl与HUB Organoids B.V.联系，以获取商业用途许可或HUB Organoids B.V.许可的相关说明。
分类
专用培养基
细胞类型
肠道细胞
种属
人
应用
细胞培养，分化，扩增，培养，类器官培养
品牌
IntestiCult
研究领域
疾病建模，上皮细胞研究，干细胞生物学
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 (62)
文献 (33)
Interferon gamma decreases intestinal epithelial aquaporin 3 expression through downregulation of constitutive transcription.
Journal of molecular medicine (Berlin,Germany) 2018 oct
Abstract
Aquaporin (AQP) 3 expression is altered in inflammatory bowel diseases,although the exact mechanisms regulating AQP abundance are unclear. Although interferon gamma (IFNgamma) is centrally involved in intestinal inflammation,the effect of this cytokine on AQP3 expression remains unknown. HT-29 human colonic epithelial cells were treated with IFNgamma to assess AQP3 mRNA expression by real-time RT-PCR and functional protein expression through the uptake of radiolabelled glycerol. Transient knockdown of signal transducer and activator of transcription 1 (STAT1),STAT3,Sp1,and Sp3 were performed to determine the involvement of these transcription factors in the IFNgamma-induced signalling cascade. AQP3 promoter regions involved in the response to IFNgamma were assessed using a luciferase reporter system. Likewise,enteroids derived from human colonic biopsies were also treated with IFNgamma to assess for changes in AQP3 mRNA expression. IFNgamma decreased AQP3 mRNA expression in HT-29 cells in a time- and concentration-dependent manner and reduced functional AQP3 protein expression (decreased 3H-labelled glycerol uptake). IFNgamma also reduced AQP3 expression in enteroids derived from human colonic biopsies. Knockdown of STAT1 partially prevented the IFNgamma-induced downregulation of AQP3 expression,whereas STAT3 and Sp3 knockdowns resulted in increased baseline expression of AQP3 but did not alter IFNgamma-induced downregulation. Constitutive transcription of AQP3 is downregulated by IFNgamma as demonstrated using the luciferase reporter system,with Sp3 bound to the AQP3 promoter as shown by chromatin immunoprecipitation. AQP3 constitutive transcription in intestinal epithelial cells is downregulated by IFNgamma. This response requires STAT1 that is postulated to drive the downregulation of AQP3 expression through increased acetylation or decreased deacetylation the AQP3 promoter,ultimately resulting in decreased constitutive transcription of AQP3. KEY MESSAGES • IFNgamma suppresses the expression of AQP3 in intestinal epithelial cells. • Proximal AQP3 promoter elements are sufficient to drive constitutive expression and mediate the IFNgamma-induced downregulation of AQP3 mRNA expression. • IFNgamma-induced suppression of AQP3 is dependent upon STAT1 expression,but not STAT3,Sp1,or Sp3.
NOX1-derived ROS drive the expression of Lipocalin-2 in colonic epithelial cells in inflammatory conditions.
Mucosal immunology 2019 jan
Abstract
Inflammatory bowel disease (IBD) is characterized by severe and recurrent inflammation of the gastrointestinal tract,associated with altered patterns of cytokine synthesis,excessive reactive oxygen species (ROS) production,and high levels of the innate immune protein,lipocalin-2 (LCN-2),in the mucosa. The major source of ROS in intestinal epithelial cells is the NADPH oxidase NOX1,which consists of the transmembrane proteins,NOX1 and p22PHOX,and the cytosolic proteins,NOXO1,NOXA1,and Rac1. Here,we investigated whether NOX1 activation and ROS production induced by key inflammatory cytokines in IBD causally affects LCN-2 production in colonic epithelial cells. We found that the combination of TNFalpha and IL-17 induced a dramatic upregulation of NOXO1 expression that was dependent on the activation of p38MAPK and JNK1/2,and resulted into an increase of NOX1 activity and ROS production. NOX1-derived ROS drive the expression of LCN-2 by controlling the expression of IkappaBzeta,a master inducer of LCN-2. Furthermore,LCN-2 production and colon damage were decreased in NOX1-deficient mice during TNBS-induced colitis. Finally,analyses of biopsies from patients with Crohn's disease showed increased JNK1/2 activation,and NOXO1 and LCN-2 expression. Therefore,NOX1 might play a key role in mucosal immunity and inflammation by controlling LCN-2 expression.
Human Milk Oligosaccharides Increase Mucin Expression in Experimental Necrotizing Enterocolitis.
Molecular nutrition food research 2019 nov
Abstract
SCOPE Necrotizing enterocolitis (NEC) is a leading cause of morbidity and death in preterm infants,occurring more often in formula-fed than breastfed infants. Studies in both rats and humans show that human milk oligosaccharides (HMOs) lower the incidence of NEC,but the mechanism underlying such protection is currently unclear. METHODS AND RESULTS By extracting HMOs from pooled human breastmilk,the impact of HMOs on the intestinal mucin levels in a murine model of NEC are investigated. To confirm the results,the findings are validated by exposing human intestinal epithelial cells and intestinal organoids to HMOs and evaluated for mucin expression. HMO-gavage to pups increases Muc2 levels and decreases intestinal permeability to macromolecular dextran. HMO-treated cells have increased Muc2 expression,decreased bacterial attachment and dextran permeability during challenge by enteric pathogens. To identify the mediators involved in HMO induction of mucins,it is demonstrated that HMOs directly induce the expression of chaperone proteins including protein disulfide isomerase (PDI). Suppression of PDI activity removes the protective effects of HMOs on barrier function in vitro as well as NEC protection in vivo. CONCLUSIONS Taken together,the results provide insights to the possible mechanisms by which HMOs protect the neonatal intestine through upregulation of mucins.
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法律声明:
This product was developed under a license to intellectual property owned by Hubrecht Organoid Technology (HUB). This product is sold for research use only. Purchase of this product does not include the right to use it for drug screening aiming for commercial gain, equipment validation, biobanking, or for other commercial purposes. Purchasers wishing to use the product for purposes other than basic research use should contact HUB at www.huborganoids.nl to obtain a further license. Purchasers may apply for a License from HUB, which will not be unreasonably withheld by HUB. 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.
This product was developed under a license to intellectual property owned by Hubrecht Organoid Technology (HUB). This product is sold for research use only. Purchase of this product does not include the right to use it for drug screening aiming for commercial gain, equipment validation, biobanking, or for other commercial purposes. Purchasers wishing to use the product for purposes other than basic research use should contact HUB at www.huborganoids.nl to obtain a further license. Purchasers may apply for a License from HUB, which will not be unreasonably withheld by HUB. 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.
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