The myosin-activated thin filament regulatory state, M⁻-open: a link to hypertrophic cardiomyopathy (HCM). (Q38205172)

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14 March 2020

title

The myosin-activated thin filament regulatory state, M⁻-open: a link to hypertrophic cardiomyopathy (HCM) (English)

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hypertrophic cardiomyopathy

14 March 2020

main subject

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2

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14 March 2020

author name string

Sherwin S Lehrer

series ordinal

1

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14 March 2020

publication date

17 April 2014

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Journal of Muscle Research & Cell Motility

14 March 2020

published in

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14 March 2020

volume

35

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14 March 2020

issue

2

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14 March 2020

page(s)

153-160

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Enhanced active cross-bridges during diastole: molecular pathogenesis of tropomyosin's HCM mutations

14 March 2020

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α-Tropomyosin with a D175N or E180G mutation in only one chain differs from tropomyosin with mutations in both chains

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Ca2 -dependent photocrosslinking of tropomyosin residue 146 to residues 157-163 in the C-terminal domain of troponin I in reconstituted skeletal muscle thin filaments

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A mutation in TNNC1-encoded cardiac troponin C, TNNC1-A31S, predisposes to hypertrophic cardiomyopathy and ventricular fibrillation

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A troponin T mutation that causes infantile restrictive cardiomyopathy increases Ca2 sensitivity of force development and impairs the inhibitory properties of troponin

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A functional and structural study of troponin C mutations related to hypertrophic cardiomyopathy.

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12 December 2020

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10.1007/S10974-014-9383-Z

Identifiers

DOI

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https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:24740688 AND SRC:MED&resulttype=core&format=json

Dimensions Publication ID

14 March 2020

1039746425

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