Functional analysis of myosin mutations that cause familial hypertrophic cardiomyopathy
Journal Article
Overview
publication date
- December 1, 1998
has subject area
- Adenosine Triphosphatases
- Adenosine Triphosphatases - Molecular Motor Proteins
- Adenosine Triphosphatases - Myosin Heavy Chains
- Adenosine Triphosphatases - Myosins
- Alleles
- Animals
- Aortic Valve Disease - Cardiomyopathy, Hypertrophic
- Binding Sites
- Biological Science Disciplines - Biophysics
- Biophysical Phenomena
- Biophysical Phenomena - Biomechanical Phenomena
- Birds - Chickens
- Cardiomyopathies - Cardiomyopathy, Hypertrophic
- Cell Line, Transformed - COS Cells
- Cytoskeletal Proteins - Actins
- Cytoskeletal Proteins - Myosin Heavy Chains
- Cytoskeletal Proteins - Myosins
- Fibroblasts - COS Cells
- Galliformes - Chickens
- Humans
- Macromolecular Substances - Actins
- Macromolecular Substances - Myosin Heavy Chains
- Macromolecular Substances - Myosins
- Mechanical Phenomena - Biomechanical Phenomena
- Models, Molecular
- Multiprotein Complexes - Molecular Motor Proteins
- Muscle Proteins - Actins
- Muscle Proteins - Myosin Heavy Chains
- Muscle Proteins - Myosins
- Mutation
- Nucleic Acids, Nucleotides, and Nucleosides - Adenosine Triphosphate
- Phenotype
- Physics - Biophysics
- Protein Conformation
- Purines - Adenosine Triphosphate
- Rats
- Recombinant Proteins
- Ribonucleotides - Adenosine Triphosphate
has restriction
- hybrid
Date in CU Experts
- September 6, 2013 4:09 AM
Full Author List
- Roopnarine O; Leinwand LA
author count
- 2
citation count
- 44
published in
Other Profiles
International Standard Serial Number (ISSN)
- 0006-3495
Digital Object Identifier (DOI)
Additional Document Info
start page
- 3023
end page
- 3030
volume
- 75
issue
- 6