A role for actin flexibility in thin filament-mediated contractile regulation and myopathy

The α-cardiac actin M305L hypertrophic cardiomyopathy-causing mutation is located near residues that help confine tropomyosin to an inhibitory position along thin filaments. Here the authors assessed M305L actin in vivo, in vitro, and in silico to characterize emergent pathological properties and de...

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Autores principales:	Meera C. Viswanathan, William Schmidt, Peter Franz, Michael J. Rynkiewicz, Christopher S. Newhard, Aditi Madan, William Lehman, Douglas M. Swank, Matthias Preller, Anthony Cammarato
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2020
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/05ebaf72ecab4ca79c70cc1236244ddd
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spelling	oai:doaj.org-article:05ebaf72ecab4ca79c70cc1236244ddd2021-12-02T15:54:49ZA role for actin flexibility in thin filament-mediated contractile regulation and myopathy10.1038/s41467-020-15922-52041-1723https://doaj.org/article/05ebaf72ecab4ca79c70cc1236244ddd2020-05-01T00:00:00Zhttps://doi.org/10.1038/s41467-020-15922-5https://doaj.org/toc/2041-1723The α-cardiac actin M305L hypertrophic cardiomyopathy-causing mutation is located near residues that help confine tropomyosin to an inhibitory position along thin filaments. Here the authors assessed M305L actin in vivo, in vitro, and in silico to characterize emergent pathological properties and define the mechanistic basis of disease.Meera C. ViswanathanWilliam SchmidtPeter FranzMichael J. RynkiewiczChristopher S. NewhardAditi MadanWilliam LehmanDouglas M. SwankMatthias PrellerAnthony CammaratoNature PortfolioarticleScienceQENNature Communications, Vol 11, Iss 1, Pp 1-15 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Meera C. Viswanathan William Schmidt Peter Franz Michael J. Rynkiewicz Christopher S. Newhard Aditi Madan William Lehman Douglas M. Swank Matthias Preller Anthony Cammarato A role for actin flexibility in thin filament-mediated contractile regulation and myopathy
description	The α-cardiac actin M305L hypertrophic cardiomyopathy-causing mutation is located near residues that help confine tropomyosin to an inhibitory position along thin filaments. Here the authors assessed M305L actin in vivo, in vitro, and in silico to characterize emergent pathological properties and define the mechanistic basis of disease.
format	article
author	Meera C. Viswanathan William Schmidt Peter Franz Michael J. Rynkiewicz Christopher S. Newhard Aditi Madan William Lehman Douglas M. Swank Matthias Preller Anthony Cammarato
author_facet	Meera C. Viswanathan William Schmidt Peter Franz Michael J. Rynkiewicz Christopher S. Newhard Aditi Madan William Lehman Douglas M. Swank Matthias Preller Anthony Cammarato
author_sort	Meera C. Viswanathan
title	A role for actin flexibility in thin filament-mediated contractile regulation and myopathy
title_short	A role for actin flexibility in thin filament-mediated contractile regulation and myopathy
title_full	A role for actin flexibility in thin filament-mediated contractile regulation and myopathy
title_fullStr	A role for actin flexibility in thin filament-mediated contractile regulation and myopathy
title_full_unstemmed	A role for actin flexibility in thin filament-mediated contractile regulation and myopathy
title_sort	role for actin flexibility in thin filament-mediated contractile regulation and myopathy
publisher	Nature Portfolio
publishDate	2020
url	https://doaj.org/article/05ebaf72ecab4ca79c70cc1236244ddd
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A role for actin flexibility in thin filament-mediated contractile regulation and myopathy

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