Abstract
Non-muscle myosin 2A (NM2A) is a ubiquitously-expressed myosin important for organizing cellular actin filaments. Upon regulatory light chain dephosphorylation, NM2A forms a compact, inactive (‘shutdown’) state, termed 10S, in which the filament-forming tail interacts with the myosin heads. Over 80 mutations in the NM2A heavy chain-encoding gene (MYH9) have been described, collectively causing an autosomal-dominant disorder. Two-thirds of these mutations occur in the coiled-coil tail, composed of the proximal subfragment-2 and distal light meromyosin (LMM).
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