Myosin Heavy Chain 10, Non Muscle (MYH10)

Myh10 was abundantly expressed in mouse brain and testis. It was also expressed in heart, lung, liver, and kidney, but not in skeletal muscle or spleen.Actin-activated MgATPase activity was decreased in MYH10 with either an asn97-to-lysine substitution, which is homologous to the N93K mutation in MYH9 that causes May-Hegglin anomaly , or an arg709-to-cysteine substitution, which causes developmental defects in brain and heart when present in mouse Myh10. The ability of MYH10 heavy meromyosin to support the movement of actin filaments over an MYH10-coated surface was reduced in heavy meromyosin with the N97K mutation and eliminated with the R709C mutation. Kinetic analysis indicated that the R709C mutation resulted in extremely tight affinity between MYH10 heavy meromyosin and ADP, reducing the rate of ADP release.