IntestiCultâ„¢ Organoid Growth Medium (Mouse)
Cell culture medium for establishment and maintenance of mouse intestinal organoids
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Products for Your Protocol
To see all required products for your protocol, please consult the
Protocols and Documentation.
- Gentle Cell Dissociation Reagent
cGMP, enzyme-free cell dissociation reagent
- Organoid Culture Plates
Cell culture plates for easy and reproducible generation of organoids
- DMEM/F-12 with 15 mM HEPES
Dulbecco's Modified Eagle's Medium/Nutrient Ham's Mixture F-12 (DMEM/F-12) with 15 mM HEPES buffer
- Mouse Intestinal Organoids
Cryopreserved mouse intestinal epithelial organoids for establishment of organoid cultures
Overview
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 (39)
Publications (130)
Ageâ€Associated Impairment of Paneth Cells Driven by microRNAâ€152 Promotes Intestinal Epithelial Vulnerability to Pathological Stress
Aging Cell 2026 May
Abstract
ABSTRACTAdvanced age is a wellâ€known risk factor for severe complications in surgical patients with critical illnesses, partly due to declined intestinal mucosal defense, but the underlying mechanism remains largely unknown. Our study provided direct evidence from older human and mouse small intestines of the adverse impact of aging on Paneth cell functionality by impaired mitochondrial metabolism. Mechanistic investigation revealed a specific elevation of Paneth cell enriched microRNAâ€152 (miRâ€152) in aging small intestinal epithelium. Increased miRâ€152 impaired Paneth cells of aging small intestine by inhibiting mitochondrial protein Prohibitin1 (PHB1) expression and disrupting mitochondrial respiration. Moreover, the levels of circHIPK3, an intestinal circular RNA that counters the function of miRâ€152, also declined in older intestines, further enabling miRâ€152â€mediated deterioration in Paneth cell function. Conversely, antagonizing miRâ€152 improved mitochondrial metabolism by restoring PHB1 levels and ameliorated the functional decline of old Paneth cells. Our findings indicate that dysregulated miRâ€152 expression and activity play a central role in the loss of Paneth cell homeostasis in the aging small intestine, offering translational insights for protecting intestinal mucosal integrity in older patients. Aging associated miRâ€152 dysregulation plays a central role in the loss of Paneth cell homeostasis by inhibiting mitochondrial protein Prohibitin1 (PHB1) expression, which contributes to increased small intestinal vulnerability to pathological stresses.
G9a-mediated H3K9me2 orchestrates intestinal epithelial regeneration through epigenetic silencing of cell cycle-related genes
Nature Communications 2026 Jan
Abstract
Histone modifications play an important role in intestinal homeostasis and regeneration. Here, we identify histone H3 lysine 9 di-methylation (H3K9me2) as an epigenetic regulator of intestinal epithelial repair through mass spectrometry-based screening of histone modifications. We then find that H3K9me2 and its methyltransferase G9a levels are reduced during acute injury and progressively increase during regeneration in both mouse models and human clinical samples. Genetic ablation of G9a in intestinal epithelial cells or pharmacological inhibition of its enzymatic activity substantially impairs intestinal regeneration and reduces survival following irradiation. Mechanistically, integrative genomic analyses reveal that G9a-mediated H3K9me2 suppresses chromatin accessibility and transcriptional activity of cell cycle arrest genes, including Rb1cc1, Rb1, Cdkn1a, and Pten, thereby promoting intestinal stem cell proliferation. Furthermore, we elucidate that IL-4-STAT6 signaling controls G9a expression during regeneration, i.e., IL-4 upregulation leads to STAT6 phosphorylation and subsequent transcriptional activation of G9a. These findings establish the IL-4-STAT6-G9a-H3K9me2 regulatory axis as a critical epigenetic mechanism controlling intestinal regeneration with therapeutic potential for gastrointestinal disorders. Here they show that G9a-mediated H3K9me2 regulates intestinal homeostasis and injury repair through repression of cell cycle arrest genes in both mouse and human.
A loss-of-function human ADAR variant activates innate immune response and promotes bowel inflammation
Nature Communications 2025 Sep
Abstract
Inflammatory bowel disease (IBD) arises from genetic-environmental interactions. Adenosine deaminases acting on RNA 1 (ADAR), an RNA-editing enzyme converting adenosine (A) to inosine (I), is essential for tissue homeostasis. Here we report that intestinal ADAR deficiency contributes to IBD pathogenesis in humans with reduced ADAR expression in patient intestinal crypts. Genetic or pharmacological inhibition of ADAR in mice causes spontaneous ileitis and colitis. Organoid studies show that ADAR loss leads to double-strand RNA (dsRNA) and endogenous retroviruses (ERVs) accumulation, disrupting intestinal homeostasis via melanoma differentiation-associated protein 5 (MDA5)-mediated dsRNA sensing and Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling. Editome analyses identify Mda5 as an ADAR target, and edited Mda5 exhibits impaired dsRNA sensing. The human ADAR p.N173S mutation is a loss-of-function variant that fails to rescue IBD in intestinal Adar deficient mice, whereas JAK1/2 inhibitor Ruxolitinib attenuates IBD. We conclude that the ADAR-dsRNA/ERVs-MDA5-JAK/STAT axis is a potential therapeutic target for IBD. Environmental and genetic factors affect the pathogenesis of inflammatory bowel disease (IBD). Here the authors show a loss of function Adenosine deaminases acting on RNA 1 (ADAR) variant that results in accumulation of dsRNA which is sensed by MDA5 and promotes bowel inflammation.
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Legal Statement:
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.
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.
Quality Statement:
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 º£½ÇÆƽâ°æ, REFER TO WWW.º£½ÇÆƽâ°æ.COM/COMPLIANCE.
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 º£½ÇÆƽâ°æ, REFER TO WWW.º£½ÇÆƽâ°æ.COM/COMPLIANCE.
Safety Statement:
CA WARNING: This product can expose you to Progesterone which is known to the State of California to cause cancer. For more information go to
