IntestiCult™ Organoid Growth Medium (Mouse)

Cell culture medium for establishment and maintenance of mouse intestinal organoids

IntestiCult™ Organoid Growth Medium (Mouse)

Cell culture medium for establishment and maintenance of mouse intestinal organoids

IntestiCult™ Organoid Growth Medium (Mouse)
1 Kit
359 USD
Catalog # 06005

Cell culture medium for establishment and maintenance of mouse intestinal organoids

Product Advantages


  • Convenient, in vitro system that recapitulates the identity and organization of the adult intestinal epithelium, including intra- and intercellular signaling, self-propagating stem cell niche and functional transport into and out of the lumen

  • Serum-free and defined medium formulation that delivers consistent results

  • Enables generation of intestinal organoids in less than one week

  • Simple format and easy-to-use protocol

What's Included

  • IntestiCult™ OGM Mouse Basal Medium, 90 mL
  • IntestiCult™ OGM Mouse Supplement 1, 5 mL
  • IntestiCult™ OGM Mouse Supplement 2, 5 mL
Products for Your Protocol
To see all required products for your protocol, please consult the Protocols and Documentation.

Overview

IntestiCult™ Organoid Growth Medium (Mouse) is a defined, serum-free cell culture medium for efficient establishment and long-term maintenance of mouse intestinal organoids.These organoids, or “mini-guts”, provide a convenient in vitro organotypic culture system for studying both the small and large intestinal epithelium and associated stem cell dynamics. Organoids grown in IntestiCult™ feature a polarized epithelium that contains all of the known cell types of the adult intestinal epithelium. Individual intestinal crypts rapidly form organoids when cultured in IntestiCult™ Organoid Growth Medium (Mouse). Applications of these cultures include studying the development and function of the normal and tumorigenic intestinal epithelium, modeling intestinal disease, and investigating stem cell properties and regenerative therapy approaches. Organoid culture enables convenient in vitro characterization of a system with strong physiological relevance to the adult intestine.
Subtype
Specialized Media
Cell Type
Intestinal Cells
Species
Mouse
Application
Cell Culture, Differentiation, Expansion, Maintenance, Organoid Culture
Brand
IntestiCult
Area of Interest
Cancer, Disease Modeling, Drug Discovery and Toxicity Testing, Epithelial Cell Biology, Stem Cell Biology
Formulation
Serum-Free

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 #
06005
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
06005
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
06005
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Catalog #
06005
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

Educational Materials (41)

Brochure

Publications (95)

Iroquois Homeobox Protein 2 Identified as a Potential Biomarker for Parkinson's Disease. H. Sim et al. International journal of molecular sciences 2020 may

Abstract

The diagnosis of Parkinson's disease (PD) is initiated after the occurrence of motor symptoms, such as resting tremors, rigidity, and bradykinesia. According to previous reports, non-motor symptoms, notably gastrointestinal dysfunction, could potentially be early biomarkers in PD patients as such symptoms occur earlier than motor symptoms. However, connecting PD to the intestine is methodologically challenging. Thus, we generated in vitro human intestinal organoids from PD patients and ex vivo mouse small intestinal organoids from aged transgenic mice. Both intestinal organoids (IOs) contained the human LRRK2 G2019S mutation, which is the most frequent genetic cause of familial and sporadic PD. By conducting comprehensive genomic comparisons with these two types of IOs, we determined that a particular gene, namely, Iroquois homeobox protein 2 (IRX2), showed PD-related expression patterns not only in human pluripotent stem cell (PSC)-derived neuroectodermal spheres but also in human PSC-derived neuronal cells containing dopaminergic neurons. We expected that our approach of using various cell types presented a novel technical method for studying the effects of multi-organs in PD pathophysiology as well as for the development of diagnostic markers for PD.
CRL3-SPOP ubiquitin ligase complex suppresses the growth of diffuse large B-cell lymphoma by negatively regulating the MyD88/NF-$\kappa$B signaling. X. Jin et al. Leukemia 2020 may

Abstract

Recurrent oncogenic mutations of MyD88 have been identified in a variety of lymphoid malignancies. Gain-of-function mutations of MyD88 constitutively activate downstream NF-$\kappa$B signaling pathways, resulting in increased cellular proliferation and survival. However, whether MyD88 activity can be aberrantly regulated in MyD88-wild-type lymphoid malignancies remains poorly understood. SPOP is an adaptor protein of CUL3-based E3 ubiquitin ligase complex and frequently mutated genes in prostate and endometrial cancers. In this study, we reveal that SPOP binds to and induces the nondegradative ubiquitination of MyD88 by recognizing an atypical SPOP-binding motif in MyD88. This modification blocks Myddosome assembly and downstream NF-$\kappa$B activation. SPOP is mutated in a subset of lymphoid malignancies, including diffuse large B-cell lymphoma (DLBCL). Lymphoid malignancies-associated SPOP mutants exhibited impaired binding to MyD88 and suppression of NF-$\kappa$B activation. The DLBCL-associated, SPOP-binding defective mutants of MyD88 escaped from SPOP-mediated ubiquitination, and their effect on NF-$\kappa$B activation is stronger than that of wild-type MyD88. Moreover, SPOP suppresses DLBCL cell growth in vitro and tumor xenograft in vivo by inhibiting the MyD88/NF-$\kappa$B signaling. Therefore, SPOP acts as a tumor suppressor in DLBCL. Mutations in the SPOP-MyD88 binding interface may disrupt the SPOP-MyD88 regulatory axis and promote aberrant MyD88/NF-$\kappa$B activation and cell growth in DLCBL.
Hormonal Suppression of Stem Cells Inhibits Symmetric Cell Division and Gastric Tumorigenesis. W. Chang et al. Cell stem cell 2020 may

Abstract

Cancer is believed to arise from stem cells, but mechanisms that limit the acquisition of mutations and tumor development have not been well defined. We show that a +4 stem cell (SC) in the gastric antrum, marked by expression of Cck2r (a GPCR) and Delta-like ligand 1 (DLL1), is a label-retaining cell that undergoes predominant asymmetric cell division. This +4 antral SC is Notch1low/ Numb+ and repressed by signaling from gastrin-expressing endocrine (G) cells. Chemical carcinogenesis of the stomach is associated with loss of G cells, increased symmetric stem cell division, glandular fission, and more rapid stem cell lineage tracing, a process that can be suppressed by exogenous gastrin treatment. This hormonal suppression is associated with a marked reduction in gastric cancer mutational load, as revealed by exomic sequencing. Taken together, our results show that gastric tumorigenesis is associated with increased symmetric cell division that facilitates mutation and is suppressed by GPCR signaling.

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