|Positive WB detected in||L02 cells, A431 cells|
|Positive IF detected in||HepG2 cells|
|Western Blot (WB)||WB : 1:500-1:1000|
|Immunofluorescence (IF)||IF : 1:10-1:100|
|Sample-dependent, check data in validation data gallery|
20720-1-AP targets MYO7A in WB, IF, ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, zebrafish|
|Host / Isotype||Rabbit / IgG|
|Full Name||myosin VIIA|
|Calculated molecular weight||254 kDa|
|Observed molecular weight||160-255 kDa|
|GenBank accession number||NM_000260|
|Gene ID (NCBI)||4647|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage. 20ul sizes contain 0.1% BSA.|
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.
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