ArticleGastroenterology2018
Loss of MYO5B Leads to Reductions in Na
Article in Gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 77 citations in OpenAlex.
- MYO5B deficiency is associated with altered MUC13 localization and DMBT1 accumulation in intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- LEF1 gene mutation impairs the intestinal barrier and causes diarrhea.Molecular and cellular pediatrics · 2026Article
- Myosin VB is critical for progenitor cell identity and function in the intestine.Stem cell reports · 2026Article
- Microvillus inclusion disease-associated MYO5B deficiency impairs endosome-to-mitochondrion iron transfer.Gastroenterology report · 2026Article
- Tannic acid-mediated gut microbes for enhanced intestinal immunity in Escherichia coli-challenged weaned piglets.Journal of animal science · 2026Article
- Microvillus Inclusion Disease: Successful Treatment of Severe Hyponatremia With High-Dose Fludrocortisone via a Possible Gut-Mediated Mechanism.ACG case reports journal · 2025Article
- Advances in Understanding Intestinal Homeostasis: Lessons from Inflammatory Bowel Disease and Monogenic Intestinal Disorder Pathogenesis.International journal of molecular sciences · 2025Review
- The MYO1B and MYO5B motor proteins and the sorting nexin SNX27 regulate apical targeting of membrane mucin MUC17 in enterocytes.The Biochemical journal · 2025Article
- Is LPAR5 agonist a new treatment for microvilli inclusion disease?American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Myosin Vb Traffics P-Glycoprotein to the Apical Membrane of Intestinal Epithelial Cells.Gastroenterology · 2025Article
- Case Report: A rare case of familial progressive cholestasis type 10 in an adult with heterozygous MYO5B variant.Frontiers in gastroenterology (Lausanne, Switzerland) · 2025Article
- Alterations in cellular metabolic pathway and epithelial cell maturation induced by MYO5B defects are partially reversible by LPAR5 activation.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- MYO5B gene mutations may promote the occurrence of very early onset inflammatory bowel disease: a case report.BMC medical genomics · 2024Article
- Modeling the cell biology of monogenetic intestinal epithelial disorders.The Journal of cell biology · 2024Review
- Patient-derived enteroids provide a platform for the development of therapeutic approaches in microvillus inclusion disease.The Journal of clinical investigation · 2023Article
- The genetics of monogenic intestinal epithelial disorders.Human genetics · 2023Review
- Review
- Therapy Development for Microvillus Inclusion Disease using Patient-derived Enteroids.bioRxiv : the preprint server for biology · 2023Article
- Article
- Modeling of a Novel Patient-Based MYO5B Point Mutation Reveals Insights Into MVID Pathogenesis.Cellular and molecular gastroenterology and hepatology · 2023Article
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 3 countries.
Funding
Abstract
BACKGROUND &
aimsInactivating mutations in MYO5B cause microvillus inclusion disease (MVID), but the physiological cause of the diarrhea associated with this disease is unclear. We investigated whether loss of MYO5B results in aberrant expression of apical enterocyte transporters.
methodsWe studied alterations in apical membrane transporters in MYO5B-knockout mice, as well as mice with tamoxifen-inducible, intestine-specific disruption of Myo5b (VilCre
resultsCompared to intestinal tissues from littermate controls, intestinal tissues from MYO5B-knockout mice had decreased apical localization of SLC9A3 (also called NHE3), SLC5A1 (also called SGLT1), aquaporin (AQP) 7, and sucrase isomaltase, and subapical localization of intestinal alkaline phosphatase and CDC42. However, CFTR was present on apical membranes of enterocytes from MYO5B knockout and control mice. Intestinal biopsies from patients with MVID had subapical localization of NHE3, SGLT1, and AQP7, but maintained apical CFTR. After tamoxifen administration, VilCre
conclusionsAlthough trafficking of many apical transporters is regulated by MYO5B, trafficking of CFTR is largely independent of MYO5B. Decreased apical localization of NHE3, SGLT1, DRA, and AQP7 might be responsible for dysfunctional water absorption in enterocytes of patients with MVID. Maintenance of apical CFTR might exacerbate water loss by active secretion of chloride into the intestinal lumen.
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