ArticleAmerican journal of physiology. Renal physiology2013
Myosin 1e is a component of the glomerular slit diaphragm complex that regulates actin reorganization during cell-cell contact formation in podocytes.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Steroid-Resistant Focal Segmental Glomerulosclerosis with Alport-like Glomerular Basement Membrane Lesions Due to aInternational journal of molecular sciences · 2026Article
- Class-I myosin responds to changes in membrane tension during clathrin-mediated endocytosis in human induced pluripotent stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Myosins 1e/f at the podosome base regulate podosome dynamics and promote macrophage migration.European journal of cell biology · 2025Article
- Roles of myosin 1e and the actin cytoskeleton in kidney functions and familial kidney disease.Cytoskeleton (Hoboken, N.J.) · 2024Review
- Myosin 1e deficiency affects migration of 4T1 breast cancer cells.Cytoskeleton (Hoboken, N.J.) · 2024Article
- A Systematic Compilation of Human SH3 Domains: A Versatile Superfamily in Cellular Signaling.Cells · 2023Review
- Focal segmental glomerulosclerosis and proteinuria associated with Myo1E mutations: novel variants and histological phenotype analysis.Pediatric nephrology (Berlin, Germany) · 2023Article
- Class I Myosins, molecular motors involved in cell migration and cancer.Cell adhesion & migration · 2022Article
- Review
- Long-Tailed Unconventional Class I Myosins in Health and Disease.International journal of molecular sciences · 2020Review
- Modification of an aggressive model of Alport Syndrome reveals early differences in disease pathogenesis due to genetic background.Scientific reports · 2019Article
- Human myosin 1e tail but not motor domain replaces fission yeast Myo1 domains to support myosin-I function during endocytosis.Experimental cell research · 2019Article
- Tail domains of myosin-1e regulate phosphatidylinositol signaling and F-actin polymerization at the ventral layer of podosomes.Molecular biology of the cell · 2019Article
- Phosphoinositides in the kidney.Journal of lipid research · 2019Review
- Effects of Xiaoyaosan on the Hippocampal Gene Expression Profile in Rats Subjected to Chronic Immobilization Stress.Frontiers in psychiatry · 2019Article
- Injury-induced actin cytoskeleton reorganization in podocytes revealed by super-resolution microscopy.JCI insight · 2017Article
- Development of a Functional Glomerulus at the Organ Level on a Chip to Mimic Hypertensive Nephropathy.Scientific reports · 2016Article
- Myosin 1e promotes breast cancer malignancy by enhancing tumor cell proliferation and stimulating tumor cell de-differentiation.Oncotarget · 2016Article
- Myosin-I molecular motors at a glance.Journal of cell science · 2016Review
- Podocyte endocytosis in the regulation of the glomerular filtration barrier.American journal of physiology. Renal physiology · 2015Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
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Abstract
Glomerular visceral epithelial cells, also known as podocytes, are critical to both normal kidney function and the development of kidney disease. Podocyte actin cytoskeleton and their highly specialized cell-cell junctions (also called slit diaphragm complexes) play key roles in controlling glomerular filtration. Myosin 1e (myo1e) is an actin-based molecular motor that is expressed in renal glomeruli. Disruption of the Myo1e gene in mice and humans promotes podocyte injury and results in the loss of the integrity of the glomerular filtration barrier. Here, we have used biochemical and microscopic approaches to determine whether myo1e is associated with the slit diaphragm complexes in glomerular podocytes. Myo1e was consistently enriched in the slit diaphragm fraction during subcellular fractionation of renal glomeruli and colocalized with the slit diaphragm markers in mouse kidney. Live cell imaging studies showed that myo1e was recruited to the newly formed cell-cell junctions in cultured podocytes, where it colocalized with the actin filament cables aligned with the nascent contacts. Myo1e-null podocytes expressing FSGS-associated myo1e mutant (A159P) did not efficiently assemble actin cables along new cell-cell junctions. We have mapped domains in myo1e that were critical for its localization to cell-cell junctions and determined that the SH3 domain of myo1e tail interacts with ZO-1, a component of the slit diaphragm complex and tight junctions. These findings suggest that myo1e represents a component of the slit diaphragm complex and may contribute to regulating junctional integrity in kidney podocytes.
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