Flightless I deficiency enhances wound repair by increasing cell migration and proliferation
Wound healing disorders are a therapeutic problem of increasing clinical importance involving substantial morbidity, mortality, and rising health costs. Our studies investigating flightless I (FliI), a highly conserved actin-remodelling protein, now reveal that FliI is an important regulator of wound repair whose manipulation may lead to enhanced wound outcomes. We demonstrate that FliI-deficient +/- mice are characterized by improved wound healing with increased epithetial migration and...[Show more]
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|Source:||Journal of Pathology|
|01_Cowin_Flightless_I_deficiency_2007.pdf||2.13 MB||Adobe PDF||Request a copy|
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