Abstract
Mutations in the cardiac β-myosin heavy chain gene (MYH7), and other genes encoding cardiac sarcomere proteins may cause familial hypertrophic cardiomyopathy (F-HCM), an autosomal dominant disease, characterized by myocardial hypertrophy. We analysed the MYH7 gene in three generations of a family with one borderline and four clinically verified cases of hypertrophic cardiomyopathy, and identified a mutation in exon 7 changing the 190 arginine residue into a threonine residue. The mutation is located in the ATP-binding region of the myosin head and alters the charge in the F-helix close to the phosphate-binding P-loop. The mutation may thus interfere with the coupling between ATP-hydrolysis and the transition into mechanical energy. In conclusion, the novel Arg190Thr mutation in exon 7 of the MYH7 gene is associated with the development of symptomatic myocardial hypertrophy in adults.
| Original language | English |
|---|---|
| Pages (from-to) | 745-750 |
| Number of pages | 6 |
| Journal | Journal of Molecular and Cellular Cardiology |
| Volume | 31 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Apr 1999 |
Funding
We thank Kirsten Lindboe and Morten Klockmann Nielsen for their excellent technical assistance. This work was supported by grants from The Danish Heart Foundation, the “Kong Christian den Tiendes Fond”, The Novo Nordisk Foundation and Director Emil C. Hertz and wife Inger Hertz’s foundation.
Keywords
- ATP binding
- Hypertrophic cardiomyopathy
- Mutation detection
- Myosin structure and function
- PCR-SSCP
- Sudden cardiac death
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