ArticleProceedings of the National Academy of Sciences of the United States of America2008
Calcium sensitivity of the cross-bridge cycle of Myo1c, the adaptation motor in the inner ear.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
- Pathogenic mechanism of the PLS1 gene variant in hearing loss and functional validation in a zebrafish model.Scientific reports · 2026Article
- Conserved Phosphorylation of the Myosin1e TH1 Domain Impacts Membrane Association and Function in Yeast and Worms.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Motor domain phosphorylation increases nucleotide exchange and turns MYO6 into a faster and stronger motor.Nature communications · 2024Article
- Distinct actin-tropomyosin cofilament populations drive the functional diversification of cytoskeletal myosin motor complexes.iScience · 2022Article
- Acetylation stabilises calmodulin-regulated calcium signalling.FEBS letters · 2022Article
- Actomyosin Complex.Sub-cellular biochemistry · 2022Article
- Unconventional Myosins: How Regulation Meets Function.International journal of molecular sciences · 2019Review
- Article
- N-terminal splicing extensions of the humanThe Journal of biological chemistry · 2017Article
- Kinetic adaptation of human Myo19 for active mitochondrial transport to growing filopodia tips.Scientific reports · 2017Article
- Chemomechanical regulation of myosin Ic cross-bridges: Deducing the elastic properties of an ensemble from single-molecule mechanisms.PLoS computational biology · 2017Article
- Rat Liver Enzyme Release Depends on Blood Flow-Bearing Physical Forces Acting in Endothelium Glycocalyx rather than on Liver Damage.Oxidative medicine and cellular longevity · 2017Article
- A Perspective on the Role of Myosins as Mechanosensors.Biophysical journal · 2016Article
- Structural Analysis of the Myo1c and Neph1 Complex Provides Insight into the Intracellular Movement of Neph1.Molecular and cellular biology · 2016Article
- Various Themes of Myosin Regulation.Journal of molecular biology · 2016Review
- Is Liver Enzyme Release Really Associated with Cell Necrosis Induced by Oxidant Stress?Oxidative medicine and cellular longevity · 2016Review
- Actin filaments as the fast pathways for calcium ions involved in auditory processes.Journal of biosciences · 2015Article
- Mechanochemical tuning of myosin-I by the N-terminal region.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Structure of myosin-1c tail bound to calmodulin provides insights into calcium-mediated conformational coupling.Nature structural & molecular biology · 2015Article
- Myosin light chains: Teaching old dogs new tricks.Bioarchitecture · 2014Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The class I myosin Myo1c is a mediator of adaptation of mechanoelectrical transduction in the stereocilia of the inner ear. Adaptation, which is strongly affected by Ca(2+), permits hair cells under prolonged stimuli to remain sensitive to new stimuli. Using a Myo1c fragment (motor domain and one IQ domain with associated calmodulin), with biochemical and kinetic properties similar to those of the native molecule, we have performed a thorough analysis of the biochemical cross-bridge cycle. We show that, although the steady-state ATPase activity shows little calcium sensitivity, individual molecular events of the cross-bridge cycle are calcium-sensitive. Of significance is a 7-fold inhibition of the ATP hydrolysis step and a 10-fold acceleration of ADP release in calcium. These changes result in an acceleration of detachment of the cross-bridge and a lengthening of the lifetime of the detached M-ATP state. These data support a model in which slipping adaptation, which reduces tip-link tension and allows the transduction channels to close after an excitatory stimulus, is mediated by Myo1c and modulated by the calcium transient.
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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.