Key result
The tail domain of human myosin VIIA inhibits its ATPase activity and translocation to filopodial tips, a mechanism that operates both in vitro and in vivo.
Population
In vitro and cellular models studying human myosin VIIA (HM7A)
Comparison
Tail truncation, C-terminal deletion, and… vs Full-length HM7A (HM7AFull)
Design
Preclinical
Authors
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Hypothesis-generating for Usher 1B therapies; leaves open translation from animal models to clinical interventions.
The tail domain of human myosin VIIA inhibits its ATPase activity and cellular translocation, providing mechanistic insights into human Usher syndrome type 1B.
Sakai et al. (2015) studied Human Usher syndrome type 1B. Tail domain deletion or mutation vs. Full-length human myosin VIIA (HM7AFull) was evaluated on Actin-activated ATPase activity and filopodial tip translocation. The tail domain of human myosin VIIA inhibits its ATPase activity and translocation to filopodial tips, a mechanism that operates both in vitro and in vivo.
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