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Myosin-IIIa is an unconventional myosin motor protein that also contains a protein kinase domain. It walks toward the plus end of actin filaments and is highly expressed in sensory cells, notably in the stereocilia of the inner ear and photoreceptor cells in the retina. MYO3A plays critical roles in regulating actin-rich cellular protrusions by transporting actin-bundling proteins, such as espin, to the tips of filopodia, microvilli, and stereocilia. Its activity is regulated through autophosphorylation of its kinase and motor domains, which affects both motor properties and subcellular localization. Pathogenic mutations in MYO3A are causative of hereditary forms of nonsyndromic deafness, due to impaired regulation of stereocilia length and function. No drugs currently target MYO3A directly, and it is not considered a therapeutic target, but it is a gene of clinical interest for genetic screening in hearing loss disorders.
Not applicable; there are no known drugs or therapeutic inhibitors/activators targeting MYO3A
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