Abstract:
:Myosin-binding protein C (MyBP-C) is a thick filament protein playing an essential role in muscle contraction, and MyBP-C mutations cause heart and skeletal muscle disease in millions worldwide. Despite its discovery 40 y ago, the mechanism of MyBP-C function remains unknown. In vitro studies suggest that MyBP-C could regulate contraction in a unique way--by bridging thick and thin filaments--but there has been no evidence for this in vivo. Here we use electron tomography of exceptionally well preserved muscle to demonstrate that MyBP-C does indeed bind to actin in intact muscle. This binding implies a physical mechanism for communicating the relative sliding between thick and thin filaments that does not involve myosin and which could modulate the contractile process.
journal_name
Proc Natl Acad Sci U S Aauthors
Luther PK,Winkler H,Taylor K,Zoghbi ME,Craig R,Padrón R,Squire JM,Liu Jdoi
10.1073/pnas.1103216108subject
Has Abstractpub_date
2011-07-12 00:00:00pages
11423-8issue
28eissn
0027-8424issn
1091-6490pii
1103216108journal_volume
108pub_type
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