In vivo analysis of an essential myosin light chain mutation linked to familial hypertrophic cardiomyopathy

Circulation Research

Volumn 87, Issue 4, 2000, Pages 296-302

  Sanbe, Atsushi ^a   Nelson, David ^a   Gulick, James ^a   Setser, Elizabeth ^a   Osinska, Hanna ^a   Wang, Xuejun ^a   Hewett, Timothy E ^a   Klevitsky, Raisa ^a   Hayes, Eric ^b   Warshaw, David M ^b   Robbins, Jeffrey ^a,c  

^a CINCINNATI CHILDREN S HOSPITAL RESEARCH FOUNDATION   (United States)

^b UNIVERSITY OF VERMONT   (United States)

^c Division of Molecular Cardiovascular Biology   (United States)

Author keywords

Heart; Hypertrophy; Mouse; Muscle; Myosin

Indexed keywords

MYOSIN LIGHT CHAIN;

ANIMAL TISSUE; ARTICLE; GENE MUTATION; HYPERTROPHIC CARDIOMYOPATHY; MOUSE; NONHUMAN; POINT MUTATION; PRIORITY JOURNAL; TRANSGENIC MOUSE;

EID: 0034683061     PISSN: 00097330     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.RES.87.4.296     Document Type: Article

References (18)

1. Molecular genetic studies of familial hypertrophic cardiomyopathy
2. Molecular genetics of inherited cardiomyopathies
3. The management of hypertrophic cardiomyopathy
4. Mutations in either the essential or regulatory light chains of myosin are associated with a rare myopathy in human heart and skeletal muscle
5. The stretch-activation response may be critical to the proper functioning of the mammalian heart
6. Identification of two novel mutations in the ventricular regulatory myosin light chain gene (MYL2) associated with familial and classical forms of hypertrophic cardiomyopathy
7. Transgenic over-expression of a motor protein at high levels results in severe cardiac pathology
8. Intracompartmental sorting of essential myosin light chains: Molecular dissection and in vivo monitoring by epitope tagging
9. Myosin light chain replacement in the heart
10. Transgenic remodeling of the mammalian heart
11. Abnormal cardiac structure and function in mice expressing nonphosphorylatable cardiac regulatory myosin light chain 2
12. Cardiac troponin T mutations result in allelespecific phenotypes in a mouse model for hypertrophic cardiomyopathy
13. Modulation of contractility in human cardiac hypertrophy by myosin essential light chain isoforms
14. Cardiac myosin heavy chains lacking the fight chain binding domain cause hypertrophic cardiomyopathy in mice
15. Tuning the human heart molecular motors by myosin light chains
16. Expression of proto-oncogenes and gene mutation of sarcomeric proteins in patients with hypertrophic cardiomyopathy
17. Functional significance of cardiac myosin essential light chain isoform switching in transgenic mice
18. Maximal actomyosin ATPase activity and in vitro myosin motility are unaltered in human mitral regurgitation heart failure