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Hypertrophic cardiomyopathy-causing Asp175asn and Glu180gly Tpm1 mutations shift tropomyosin strands further towards the open position during the ATPase cycle.

Abstract:

To understand the molecular mechanism by which the hypertrophic cardiomyopathy-causing Asp175Asn and Glu180Gly mutations in α-tropomyosin alter contractile regulation, we labeled recombinant wild type and mutant α-tropomyosins with 5-iodoacetamide-fluorescein and incorporated them into the ghost muscle fibers. The orientation and mobility of the probe were studied by polarized fluorimetry at different stages of the ATPase cycle. Multistep alterations in the position and mobility of wild type ...

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Publication status:
Published

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Publisher copy:
10.1016/j.bbrc.2011.02.139

Authors


Borovikov, YS More by this author
Karpicheva, OE 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:
407
Issue:
1
Pages:
197-201
Publication date:
2011-04-05
DOI:
EISSN:
1090-2104
ISSN:
0006-291X
URN:
uuid:469be785-ebdc-4b61-a034-6a94caafacf4
Source identifiers:
124319
Local pid:
pubs:124319

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