Flexibility Change in Human Cardiac α-Tropomyosin E180G Mutant: Possible Link to Cardiac Hypertrophy

Loong, Campion K. P.; Zhou, Huan‐Xiang; Chase, P. Bryant

doi:10.1016/j.bpj.2010.12.3384

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2012

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“…Hypersensitivity to Ca 2+ could overwork cardiac muscle, resulting in FHC. Preliminary data were presented in an abstract [27].…”

Section: Introductionmentioning

confidence: 99%

Familial hypertrophic cardiomyopathy related E180G mutation increases flexibility of human cardiac α‐tropomyosin

Loong¹,

Zhou²,

Chase³

2012

FEBS Letters

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α-tropomyosin (αTm) is central to Ca2+-regulation of cardiac muscle contraction. The familial hypertrophic cardiomyopathy mutation αTm E180G enhances Ca2+-sensitivity in functional assays. To investigate the molecular basis, we imaged single molecules of human cardiac αTm E180G by direct probe atomic force microscopy. Analyses of tangent angles along molecular contours yielded persistence length corresponding to ~35% increase in flexibility compared to wild-type. Increased flexibility of the mutant was confirmed by fitting end-to-end length distributions to the worm-like chain model. This marked increase in flexibility can significantly impact systolic and possibly diastolic phases of cardiac contraction, ultimately leading to hypertrophy.

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“…Hypersensitivity to Ca 2+ could overwork cardiac muscle, resulting in FHC. Preliminary data were presented in an abstract [27].…”

Section: Introductionmentioning

confidence: 99%

Familial hypertrophic cardiomyopathy related E180G mutation increases flexibility of human cardiac α‐tropomyosin

Loong¹,

Zhou²,

Chase³

2012

FEBS Letters

Self Cite

View full text Add to dashboard Cite

show abstract

Flexibility Change in Human Cardiac α-Tropomyosin E180G Mutant: Possible Link to Cardiac Hypertrophy

Cited by 1 publication

References 0 publications

Familial hypertrophic cardiomyopathy related E180G mutation increases flexibility of human cardiac α‐tropomyosin

Familial hypertrophic cardiomyopathy related E180G mutation increases flexibility of human cardiac α‐tropomyosin

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