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Dilated cardiomyopathy mutations in alpha-tropomyosin inhibit its movement during the ATPase cycle.

Abstract:

The Glu40Lys and Glu54Lys mutations in alpha-tropomyosin cause dilated cardiomyopathy (DCM). Functional analysis has demonstrated that both mutations decrease thin filament Ca2+-sensitivity and that Glu40Lys reduces maximum activation. To understand the molecular mechanism underlying these changes, we labeled wild type alpha-tropomyosin and both mutants at Cys190 with 5-iodoacetamide-fluorescein and incorporated the labeled proteins into ghost muscle fibers. Using the polarized fluorimetry, t...

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Publication status:
Published

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Publisher copy:
10.1016/j.bbrc.2009.02.054

Authors


Borovikov, YS More by this author
Karpicheva, OE More by this author
Chudakova, GA More by this author
Robinson, P More by this author
More by this author
Institution:
University of Oxford
Department:
Oxford, MSD, RDM, Cardiovascular Medicine, BHF Centre of Research Excellence
Journal:
Biochemical and biophysical research communications
Volume:
381
Issue:
3
Pages:
403-406
Publication date:
2009-04-05
DOI:
EISSN:
1090-2104
ISSN:
0006-291X
URN:
uuid:01f04000-8621-404b-9af1-4cccedd343af
Source identifiers:
104944
Local pid:
pubs:104944

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