ArticleBiochemistry2014
BIN1 membrane curvature sensing and generation show autoinhibition regulated by downstream ligands and PI(4,5)P2.
Article in Biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Genetic Determinants of Tau-PET Imaging in Alzheimer's Disease: A Narrative Review of Genome-Wide and Candidate-Gene Studies.Journal of imaging · 2026Review
- Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer's disease.Neural regeneration research · 2026Article
- Early Stage Morphogenesis of Transverse Tubules in Rat Cardiomyocytes: The Role of pBIN1.Circulation research · 2025Article
- Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025Review
- Neurons Specialize in Presynaptic Autophagy: A Perspective to Ameliorate Neurodegeneration.Molecular neurobiology · 2025Review
- Article
- Dynamics of membrane tubulation coupled with fission by a two-component module.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- BIN1 regulates actin-membrane interactions during IRSp53-dependent filopodia formation.Communications biology · 2024Article
- Five questions on the cell-to-cell movement ofBBA advances · 2024Article
- PI(4,5)PAdvances in experimental medicine and biology · 2023Article
- Centronuclear Myopathy Caused by Defective Membrane Remodelling of Dynamin 2 and BIN1 Variants.International journal of molecular sciences · 2022Review
- Cavin4 interacts with Bin1 to promote T-tubule formation and stability in developing skeletal muscle.The Journal of cell biology · 2021Article
- Nanoscale Organization, Regulation, and Dynamic Reorganization of Cardiac Calcium Channels.Frontiers in physiology · 2021Review
- Review of PIP2 in Cellular Signaling, Functions and Diseases.International journal of molecular sciences · 2020Review
- Nanobar Array Assay Revealed Complementary Roles of BIN1 Splice Isoforms in Cardiac T-Tubule Morphogenesis.Nano letters · 2020Article
- Review
- Protein Amphipathic Helix Insertion: A Mechanism to Induce Membrane Fission.Frontiers in cell and developmental biology · 2019Review
- BAR domain proteins-a linkage between cellular membranes, signaling pathways, and the actin cytoskeleton.Biophysical reviews · 2018Review
- Dynamin 2 (DNM2) as Cause of, and Modifier for, Human Neuromuscular Disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- Mind the (sr)GAP - roles of Slit-Robo GAPs in neurons, brains and beyond.Journal of cell science · 2017Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In striated muscles, invaginations from the plasma membrane, termed transverse tubules (T-tubule), function in the excitation-contraction coupling machinery. BIN1 (isoform8) plays a critical role in the biogenesis of T-tubules. BIN1 contains an N-terminal BAR domain to sense and induce membrane curvature, an isoform8-specific polybasic motif (exon10) as the phosphoinositide binding module and a C-terminal Src homology 3 (SH3) domain for the recruitment of downstream proteins such as dynamin 2. Previous studies of N-BAR domains focused on elucidating mechanisms of membrane curvature sensing and generation (MC-S&G). Less is known about how MC-S&G is regulated. We found that the SH3 domain binds to the exon10 motif more strongly compared to the proline-rich domain (PRD) of dynamin 2. Furthermore, we found that the MC-S&G ability of full-length BIN1 is inhibited on membranes lacking PI(4,5)P2. Addition of PI(4,5)P2 in the membrane activates BIN1 to sense and induce membrane curvature. Co-presence of the SH3 domain and exon10 motif leads to the strongest phosphoinositide-mediated control of BIN1 function. Addition of SH3 domain ligand (such as PRD peptides), as well as addition of the water-soluble PI(4,5)P2 analogue, can both enhance the MC-S&G ability of BIN1 on membranes without PI(4,5)P2, indicating that the key to activate BIN1 is to disrupt the exon10-SH3 interaction. The nonsense mutation K436X, found in centronuclear myopathy (CNM) patients, abolishes SH3 domain binding with either exon10 or the PRD motif, resulting in increased membrane deformation capacity. Our results suggest an autoinhibition model for BIN1 that involves a synergistic regulation by membrane composition and protein-protein interactions.
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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.