MYO7A, also named a USH1B, is one of myosins protein which are actin-based motor molecules with ATPase activity. Unconventional myosins serve in intracellular movements. Their highly divergent tails are presumed to bind to membranous compartments, which would be moved relative to actin filaments. In retina, MYO7A might play a role in trafficking of ribbon-synaptic vesicle complexes and renewal of the outer photoreceptors disks. In inner ear, it might maintain the rigidity of stereocilia during the dynamic movements of the bundle. It is involved in hair-cell vesicle trafficking of aminoglycosides, which are known to induce ototoxicity. Defects in MYO7A are the cause of Usher syndrome type 1B (USH1B). Defects in MYO7A are the cause of deafness autosomal recessive type 2 (DFNB2). Defects in MYO7A are the cause of deafness autosomal dominant type 11 (DFNA11). The antibody is specific to MYO7A.
Western Blot:L02 Cells, 1:500-1:5000; IF: HepG2, 1:10-1:100
Type: Primary
Antigen: MYO7A
Clonality: Polyclonal
Clone:
Conjugation: Unconjugated
Epitope:
Host: Rabbit
Isotype: IgG
Reactivity: Human, Mouse, Rat