Introducing a series of topical special issues of the Journal of Muscle Research and Cell Motility

摘要: The Journal of Muscle Research aims to serve its readers not only by publishing original studies in muscle and motility structure function but also informing the state art research cell promote debate. This issue Cell Motility is first a series topical special issues that combine with review articles related specific subject we plan publish once or twice year. Further are being planned would welcome ideas for themes be covered future issues. In this issue, devoted cardiac myosinbinding protein-C. When C-protein, myosin-binding protein-C (MyBP-C) was discovered skeletal early 1970s Gerald Offer (Offer 1972; et al. 1973), MyBP-C thought merely structural protein component thick filament. Interest functions were galvanised when it found isoform, encoded MYBPC3 gene on chromosome 11, mutated cases hereditary hypertrophic cardiomyopathy (HCM) (Bonne 1995; Watkins 1995). By now, mutations second-most frequently identified cause HCM (Schlossarek 2011), carriers pathogenic mutation amounting up 4 % population Indian descent (Dhandapany 2009). It has become clear must play important roles both regulation contractility as assembly myofibrils. transcribed from three genes (MYBPC1-3), which encode slow, fast isoforms. Like many other myofibrilassociated proteins, composed hundred-residue domains intracellular immunoglobulin fibronectin families—10–11 case (Furst Gautel Otey molecular architecture shared small MyBPC homologue, protein-H (Vaughan 1993) myofibrillar proteins like myopalladin, myotilin, myomesin isogenes giant scaffold signalling titin obscurin (KontrogianniKonstantopoulos Earlier work laboratories Offer, Carl Moos, Roger Starr, Rick Moss, Polly Hofmann, Criss Hartzell others had implicated contraction interactions actin myosin filament components, possibly dynamically modulated phosphorylation cAMP calcium/calmodulin dependent kinases isoform (see literature). elucidation primary isoforms pinpointed these sites N-terminal region within sequence distinct fibronectin-like form remainder (Einheber Fischman 1990; Furst 1992; motif since been major domain involved have localised S. B. Marston NHLI, Myocardial Function, Imperial College London, Centre Translational Experimental Medicine, London W12 0NN, UK e-mail: S.marston@imperial.ac.uk