Differential cross-bridge kinetics of FHC myosin mutations R403Q and R453C in heterozygous mouse myocardium.

@article{Palmer2004DifferentialCK,
  title={Differential cross-bridge kinetics of FHC myosin mutations R403Q and R453C in heterozygous mouse myocardium.},
  author={Bradley M. Palmer and David E. Fishbaugher and Joachim P. Schmitt and Yuan Wang and Norman R. Alpert and Christine E Seidman and Jonathan G Seidman and Peter Vanburen and David W. Maughan},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2004},
  volume={287 1},
  pages={
          H91-9
        }
}
The kinetic effects of the cardiac myosin point mutations R403Q and R453C, which underlie lethal forms of familial hypertrophic cardiomyopathy (FHC), were assessed using isolated myosin and skinned strips taken from heterozygous (R403Q/+ and R453C/+) male mouse hearts. Compared with wild-type (WT) mice, actin-activated ATPase was increased by 38% in R403Q/+ and reduced by 45% in R453C/+, maximal velocity of regulated thin filament (V(RTF)) in the in vitro motility assay was increased by 8% in… CONTINUE READING

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