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Publication : Nonmuscle myosin IIA facilitates vesicle trafficking for MG53-mediated cell membrane repair.

First Author  Lin P Year  2012
Journal  FASEB J Volume  26
Issue  5 Pages  1875-83
PubMed ID  22253476 Mgi Jnum  J:183293
Mgi Id  MGI:5318176 Doi  10.1096/fj.11-188599
Citation  Lin P, et al. (2012) Nonmuscle myosin IIA facilitates vesicle trafficking for MG53-mediated cell membrane repair. FASEB J 26(5):1875-83
abstractText  Repair of injury to the plasma membrane is an essential mechanism for maintenance of cellular homeostasis and integrity that involves coordinated movement of intracellular vesicles to membrane injury sites to facilitate patch formation. We have previously identified MG53 as an essential component of the cell membrane repair machinery. In order for MG53 and intracellular vesicles to translocate to membrane injury sites, motor proteins must be involved. Here, we show that nonmuscle myosin type IIA (NM-IIA) interacts with MG53 to regulate vesicle trafficking during cell membrane repair. In cells that are deficient for NM-IIA expression, MG53 cannot translocate to acute injury sites, whereas rescue of NM-IIA expression in these cells can restore MG53-mediated membrane repair. Compromised cell membrane repair is observed in cells with RNAi-mediated knockdown of NM-IIA expression, or following pharmacological alteration of NM-IIA motor function. Together, our data reveal NM-IIA as a key cytoskeleton motor protein that facilitates vesicle trafficking during MG53-mediated cell membrane repair.-Lin, P., Zhu, H., Cai, C., Wang, X., Cao, C., Xiao, R., Pan, Z., Weisleder, N., Takeshima, H., Ma, J. Nonmuscle myosin IIA facilitates vesicle trafficking for MG53-mediated cell membrane repair.
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