| Literature DB >> 22057632 |
Steven Marston1, O'Neal Copeland, Katja Gehmlich, Saskia Schlossarek, Lucie Carrier, Lucie Carrrier.
Abstract
It is well established that MYBPC3 mutations are the most common cause of hypertrophic cardiomyopathy, accounting for about half of identified mutations. However, when compared with mutations in other myofibrillar proteins that cause hypertrophic cardiomyopathy, MYBPC3 mutations seem to be the odd one out. The most striking characteristic of HCM mutations in MYBPC3 is that many are within introns and are predicted to cause aberrant splicing leading to a frameshift and a premature chain termination, yet the truncated peptides have never been identified in human heart tissue carrying these mutations. Instead of expression of a poison peptide we consistently observe haploinsufficiency of MyBP-C in MYBPC3 mutant human heart muscle. In this review we investigate the mechanism for MyBP-C haploinsufficiency and consider how this haploinsufficiency could cause hypertrophic cardiomyopathy.Entities:
Mesh:
Substances:
Year: 2011 PMID: 22057632 DOI: 10.1007/s10974-011-9268-3
Source DB: PubMed Journal: J Muscle Res Cell Motil ISSN: 0142-4319 Impact factor: 2.698