ArticleThe Journal of cell biology2015
Cargo-selective apical exocytosis in epithelial cells is conducted by Myo5B, Slp4a, Vamp7, and Syntaxin 3.
Article in The Journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 102 citations in OpenAlex.
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- Unconventional Protein Transport Across the Golgi Ribbon.Sub-cellular biochemistry · 2026Review
- Congenital enteropathy caused by ezrin deficiency.Human genetics · 2025Article
- Plant viruses exploit insect salivary GAPDH to modulate plant defenses.Nature communications · 2024Article
- Actomyosin organelle functions of SPIRE actin nucleators precede animal evolution.Communications biology · 2024Article
- Modeling the cell biology of monogenetic intestinal epithelial disorders.The Journal of cell biology · 2024Review
- Basement membrane diversification relies on two competitive secretory routes defined by Rab10 and Rab8 and modulated by dystrophin and the exocyst complex.PLoS genetics · 2024Article
- Patient-derived enteroids provide a platform for the development of therapeutic approaches in microvillus inclusion disease.The Journal of clinical investigation · 2023Article
- Article
- The genetics of monogenic intestinal epithelial disorders.Human genetics · 2023Review
- Spatial organization of lysosomal exocytosis relies on membrane tension gradients.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Therapy Development for Microvillus Inclusion Disease using Patient-derived Enteroids.bioRxiv : the preprint server for biology · 2023Article
- A CRISPR screen in intestinal epithelial cells identifies novel factors for polarity and apical transport.eLife · 2023Article
- Apical-basal polarity and the control of epithelial form and function.Nature reviews. Molecular cell biology · 2022Review
- Fetal Bowel Abnormalities Suspected by Ultrasonography in Microvillus Inclusion Disease: Prevalence and Clinical Significance.Journal of clinical medicine · 2022Article
- Loss of Serum Glucocorticoid-Inducible Kinase 1 SGK1 Worsens Malabsorption and Diarrhea in Microvillus Inclusion Disease (MVID).Journal of clinical medicine · 2022Article
- SMGL-1/NBAS acts as a RAB-8 GEF to regulate unconventional protein secretion.The Journal of cell biology · 2022Article
- Intercellular transfer of miR-200c-3p impairs the angiogenic capacity of cardiac endothelial cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- UNC45A deficiency causes microvillus inclusion disease-like phenotype by impairing myosin VB-dependent apical trafficking.The Journal of clinical investigation · 2022Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the motor protein Myosin Vb (Myo5B) or the soluble NSF attachment protein receptor Syntaxin 3 (Stx3) disturb epithelial polarity and cause microvillus inclusion disease (MVID), a lethal hereditary enteropathy affecting neonates. To understand the molecular mechanism of Myo5B and Stx3 interplay, we used genome editing to introduce a defined Myo5B patient mutation in a human epithelial cell line. Our results demonstrate a selective role of Myo5B and Stx3 for apical cargo exocytosis in polarized epithelial cells. Apical exocytosis of NHE3, CFTR (cystic fibrosis transmembrane conductance regulator), and GLUT5 required an interaction cascade of Rab11, Myo5B, Slp4a, Munc18-2, and Vamp7 with Stx3, which cooperate in the final steps of this selective apical traffic pathway. The brush border enzymes DPPIV and sucrase-isomaltase still correctly localize at the apical plasma membrane independent of this pathway. Hence, our work demonstrates how Myo5B, Stx3, Slp4a, Vamp7, Munc18-2, and Rab8/11 cooperate during selective apical cargo trafficking and exocytosis in epithelial cells and thereby provides further insight into MVID pathophysiology.
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