ArticleProceedings of the National Academy of Sciences of the United States of America2015
Myosin VI deafness mutation prevents the initiation of processive runs on actin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Direct Observation of Nanometer-Sized Steps of Single Myosin VI Molecules in Living Cells.Nano letters · 2026Article
- Understanding hypertrophic cardiomyopathy and its regulation by myosin drugs.Protein science : a publication of the Protein Society · 2025Article
- How Omecamtiv Modulates Myosin Motion.Biochemistry · 2025Article
- On the Control of Directionality of Myosin.Journal of the American Chemical Society · 2024Article
- Motor domain phosphorylation increases nucleotide exchange and turns MYO6 into a faster and stronger motor.Nature communications · 2024Article
- Functional Characterization of theInternational journal of molecular sciences · 2022Article
- Myosin modulators: emerging approaches for the treatment of cardiomyopathies and heart failure.The Journal of clinical investigation · 2022Review
- An intermediate along the recovery stroke of myosin VI revealed by X-ray crystallography and molecular dynamics.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Myosin VI-Dependent Actin Cages Encapsulate Parkin-Positive Damaged Mitochondria.Developmental cell · 2018Article
- Mechanistic and structural basis for activation of cardiac myosin force production by omecamtiv mecarbil.Nature communications · 2017Article
- Kinematics of the lever arm swing in myosin VI.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Filopodia formation and endosome clustering induced by mutant plus-end-directed myosin VI.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Loss of cargo binding in the human myosin VI deafness mutant (R1166X) leads to increased actin filament binding.The Biochemical journal · 2016Article
- Kinetic Adaptations of Myosins for Their Diverse Cellular Functions.Traffic (Copenhagen, Denmark) · 2016Review
- The acquisition of mechano-electrical transducer current adaptation in auditory hair cells requires myosin VI.The Journal of physiology · 2016Article
- Force-producing ADP state of myosin bound to actin.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Calcium can mobilize and activate myosin-VI.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in the reverse-direction myosin, myosin VI, are associated with deafness in humans and mice. A myosin VI deafness mutation, D179Y, which is in the transducer of the motor, uncoupled the release of the ATP hydrolysis product, inorganic phosphate (Pi), from dependency on actin binding and destroyed the ability of single dimeric molecules to move processively on actin filaments. We observed that processive movement is rescued if ATP is added to the mutant dimer following binding of both heads to actin in the absence of ATP, demonstrating that the mutation selectively destroys the initiation of processive runs at physiological ATP levels. A drug (omecamtiv) that accelerates the actin-activated activity of cardiac myosin was able to rescue processivity of the D179Y mutant dimers at physiological ATP concentrations by slowing the actin-independent release of Pi. Thus, it may be possible to create myosin VI-specific drugs that rescue the function of deafness-causing mutations.
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