Myosin VI (MYO6)

Myosin VI (MYO6) is an unconventional myosin motor protein that distinctively moves towards the minus (pointed) end of actin filaments, a property unique among the myosin superfamily[1][4]. It converts ATP hydrolysis into mechanical work to power the movement of vesicles and organelles within cells, playing key roles in endocytosis, exocytosis, autophagy, and cytoskeletal organization[1][2][3]. MYO6 functions both as a dimeric transporter (moving cargo along actin filaments) and as a monomeric anchor or tether (stabilizing cellular structures)[2][4]. It is essential for the maintenance and organization of specialized actin-based structures, such as stereocilia in inner ear hair cells (relevant for hearing) and actin-rich structures involved in spermatogenesis (impacting fertility)[1][4]. Genetic mutations or loss-of-function in MYO6 are established causes of hereditary forms of deafness and are implicated in male infertility and several cancers[1][4]. The protein interacts with various adaptors, such as GIPC1 and TOM1, regulating its functions in endosomal trafficking and autophagy[1][2][3]. There are currently no known drugs that specifically target Myosin VI, and it is not an established pharmacological target for approved therapeutics. However, its roles in cancer and hearing loss have prompted interest as a potential therapeutic target[4]. No validated biomarkers or drugs are reported for patient selection specific to MYO6 as of now[1][4].

Other names

Unconventional myosin-VIKIAA0389Unconventional myosin-6DFNA22DFNB37