ArticleThe Journal of experimental medicine2022
Transit-amplifying cells control R-spondins in the mouse crypt to modulate intestinal stem cell proliferation.
Article in The Journal of experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed.
- Single-Cell RNA Sequencing Reveals Disrupted Stromal-Epithelial Crosstalk Impairs Gut Barrier in Depression.Brain and behavior · 2026Article
- MINGL Quantifies Borders, Gradients, and Heterogeneity in Multicellular Tissue Organization.bioRxiv : the preprint server for biology · 2026Article
- Intestinal epithelial cells in health and disease.Tissue barriers · 2026Review
- Article
- Glutamate as a therapeutic strategy to promote liver regeneration.Clinical and translational medicine · 2025Article
- Balancing Regeneration and Resistance: Targeting DCLK1 to Mitigate Gastrointestinal Radiation Injury and Oncogenesis.Cancers · 2025Review
- p53 protein degradation redefines the initiation mechanisms and drives transitional mutations in colorectal cancer.Nature communications · 2025Article
- Review
- Pathways regulating intestinal stem cells and potential therapeutic targets for radiation enteropathy.Molecular biomedicine · 2024Review
- Article
- Review
- Article
- Transit Amplifying Cells (TACs): a still not fully understood cell population.Frontiers in bioengineering and biotechnology · 2023Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Intestinal epithelium regenerates rapidly through proliferation of intestinal stem cells (ISCs), orchestrated by potent mitogens secreted within the crypt niche. However, mechanisms regulating these mitogenic factors remain largely unknown. Here, we demonstrate that transit-amplifying (TA) cells, marked by unconventional prefoldin RPB5 interactor (URI), control R-spondin production to guide ISC proliferation. Genetic intestinal URI ablation in mice injures TA cells, reducing their survival capacity, leading to an inflamed tissue and subsequently decreasing R-spondin levels, thereby causing ISC quiescence and disruption of intestinal structure. R-spondin supplementation or restoration of R-spondin levels via cell death inhibition by c-MYC elimination or the suppression of inflammation reinstates ISC proliferation in URI-depleted mice. However, selective c-MYC and p53 suppression are required to fully restore TA cell survival and differentiation capacity and preserve complete intestinal architecture. Our data reveal an unexpected role of TA cells, which represent a signaling platform instrumental for controlling inflammatory cues and R-spondin production, essential for maintaining ISC proliferation and tissue regeneration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.