
Hypertrophic cardiomyopathy–causing mutations disrupt a key regulatory off state of myosin in thick filaments.
Models, Molecular, Binding Sites, Protein Conformation, Cardiomyopathy, Hypertrophic, Myosins, Myocardial Contraction, Actins, Ventricular Myosins, Structure-Activity Relationship, Amino Acid Substitution, Mutation, Humans, Genetic Predisposition to Disease, Research Articles, Alleles, Protein Binding
Models, Molecular, Binding Sites, Protein Conformation, Cardiomyopathy, Hypertrophic, Myosins, Myocardial Contraction, Actins, Ventricular Myosins, Structure-Activity Relationship, Amino Acid Substitution, Mutation, Humans, Genetic Predisposition to Disease, Research Articles, Alleles, Protein Binding
| selected citations These citations are derived from selected sources. This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 79 | |
| popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 1% | |
| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 1% |
