ArticleGastroenterology2024
RET Signaling Persists in the Adult Intestine and Stimulates Motility by Limiting PYY Release From Enteroendocrine Cells.
Article in Gastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Thymic Stromal Lymphopoietin-Driven B-Cell Hyperactivation Impairs Intestinal Epithelial Homeostasis Predisposing to Enterocolitis in Hirschsprung Disease.Cellular and molecular gastroenterology and hepatology · 2026Article
- GDF9, NPHS1, and RET Mark Gastric Neuroendocrine Cells and Their Disruption in a PKA-Driven Gastric Preneoplasia Model.International journal of molecular sciences · 2026Article
- Article
- Genome-wide association study of nutrient composition in meat from three two-way crossbred pig populations using whole-genome resequencing.Frontiers in veterinary science · 2026Article
- Advances in research on congenital and hereditary intestinal diseases: From molecular mechanisms to precision medicine.Intractable & rare diseases research · 2025Review
- Enteroendocrine cell differentiation: Implications for human disease.Molecular and cellular endocrinology · 2025Review
- Mesenchymal stem cell-derived apoptotic vesicles regulate irritable bowel syndrome in mice via the 5-HT brain-gut axis.Stem cell research & therapy · 2025Article
- Integration of signal transduction pathways in sensory epithelial enteroendocrine cells.Molecular biology of the cell · 2025Review
- Glial cell line derived neurotrophic factor (GDNF) induces mucosal healing via intestinal stem cell niche activation.Cell proliferation · 2025Article
- Article
- Optimization of protocols for immunohistochemical assessment of enteric nervous system in formalin fixed human tissue.bioRxiv : the preprint server for biology · 2024Article
- RET signalling controls gut motility.Nature reviews. Gastroenterology & hepatology · 2024Article
- A New Transgenic Tool to Study the Ret Signaling Pathway in the Enteric Nervous System.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsRET tyrosine kinase is necessary for enteric nervous system development. Loss-of-function RET mutations cause Hirschsprung disease (HSCR), in which infants are born with aganglionic bowel. Despite surgical correction, patients with HSCR often experience chronic defecatory dysfunction and enterocolitis, suggesting that RET is important after development. To test this hypothesis, we determined the location of postnatal RET and its significance in gastrointestinal (GI) motility.
methodsRet
resultsDistinct subsets of enteric neurons and enteroendocrine cells expressed RET in the adult intestine. RET disruption in the epithelium, rather than in enteric neurons, slowed GI motility selectively in male mice. RET kinase inhibition phenocopied this effect. Most RET
conclusionsRET signaling normally limits nutrient-dependent peptide release from L-cells and this activity is necessary for normal intestinal motility in male mice. These effects could contribute to dysmotility in HSCR, which predominantly affects males, and uncovers a mechanism that could be targeted to treat post-prandial GI dysfunction.
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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.