Key result
Mutation of three DFRXXL repeat consensus sequences in the N terminus of myosin light chain kinase significantly decreased or abolished high-affinity binding to actin-containing filaments.
Population
Purified smooth muscle myofilaments and smooth muscle cells in vivo
Design
Preclinical
Authors
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Reveals a novel MLCK actin-binding motif; extends molecular mapping of myofilament regulation but leaves in vivo roles open.
Identifies a novel actin-binding motif in smooth muscle myosin light chain kinase essential for its interaction with myofilaments.
Smith et al. (1999) studied this question. Alanine scanning mutagenesis of DFRXXL motifs in myosin light chain kinase was evaluated on Binding to actin-containing filaments. Mutation of three DFRXXL repeat consensus sequences in the N terminus of myosin light chain kinase significantly decreased or abolished high-affinity binding to actin-containing filaments.
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