ArticleGenes & development2001
Amphiphysin is necessary for organization of the excitation-contraction coupling machinery of muscles, but not for synaptic vesicle endocytosis in Drosophila.
Article in Genes & development, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
127 citing papers in PubMed, 1 synthesis or guideline pooled it, 242 citations in OpenAlex.
- Increased expression of BIN1 mediates Alzheimer genetic risk by modulating tau pathology.Molecular psychiatry · 2013Pooled it
- Linear ubiquitination triggers Amph-mediated T-tubule biogenesis.Science advances · 2026Article
- BIN1 gene replacement reverses BIN1-related centronuclear myopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025Review
- BIN1 reduction amelioratesProceedings of the National Academy of Sciences of the United States of America · 2025Article
- From function to structure: how myofibrillogenesis influences the transverse-axial tubular system development and its peculiarities.Frontiers in physiology · 2025Review
- junctionCounts: comprehensive alternative splicing analysis and prediction of isoform-level impacts to the coding sequence.NAR genomics and bioinformatics · 2024Article
- Muscle degeneration in aging Drosophila flies: the role of mechanical stress.Skeletal muscle · 2024Article
- Article
- Phospholipid scramblase 1: an essential component of the nephrocyte slit diaphragm.Cellular and molecular life sciences : CMLS · 2024Article
- Shaping transverse-tubules: central mechanisms that play a role in the cytosol zoning for muscle contraction.Journal of biochemistry · 2024Review
- MTM1 overexpression prevents and reverts BIN1-related centronuclear myopathy.Brain : a journal of neurology · 2023Article
- DNM2 levels normalization improves muscle phenotypes of a novel mouse model for moderate centronuclear myopathy.Molecular therapy. Nucleic acids · 2023Article
- REPTOR and CREBRF encode key regulators of muscle energy metabolism.Nature communications · 2023Article
- Article
- Membrane remodelling triggers maturation of excitation-contraction coupling in 3D-shaped human-induced pluripotent stem cell-derived cardiomyocytes.Basic research in cardiology · 2023Article
- GSK3α phosphorylates dynamin-2 to promote GLUT4 endocytosis in muscle cells.The Journal of cell biology · 2023Article
- Evolution of the cardiac dyad.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Centronuclear Myopathy Caused by Defective Membrane Remodelling of Dynamin 2 and BIN1 Variants.International journal of molecular sciences · 2022Review
- Mice with muscle-specific deletion of Bin1 recapitulate centronuclear myopathy and acute downregulation of dynamin 2 improves their phenotypes.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
67 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Amphiphysins 1 and 2 are enriched in the mammalian brain and are proposed to recruit dynamin to sites of endocytosis. Shorter amphiphysin 2 splice variants are also found ubiquitously, with an enrichment in skeletal muscle. At the Drosophila larval neuromuscular junction, amphiphysin is localized postsynaptically and amphiphysin mutants have no major defects in neurotransmission; they are also viable, but flightless. Like mammalian amphiphysin 2 in muscles, Drosophila amphiphysin does not bind clathrin, but can tubulate lipids and is localized on T-tubules. Amphiphysin mutants have a novel phenotype, a severely disorganized T-tubule/sarcoplasmic reticulum system. We therefore propose that muscle amphiphysin is not involved in clathrin-mediated endocytosis, but in the structural organization of the membrane-bound compartments of the excitation-contraction coupling machinery of muscles.
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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.