Flii control: balancing migration and adhesion.
Wound healing in the skin requires a compromise between adhesion and migration. Both processes include modulation of the cytoskeleton, cell-surface receptors, and receptor ligands., In this issue, Kopecki et al. demonstrate that overexpression of Flii, an actin-remodeling protein, impedes wound healing but inhibits hemidesmosome formation. In contrast, Flii deficiency results in enhanced wound healing while promoting hemidesmosome assembly. We discuss potential mechanisms that could explain how this unique gelsolin family member might regulate both stable keratinocyte adhesion and motility.
Kligys
Kristina
K
Department of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Jones
Jonathan C R
JC
D000818:Animals; D015703:Antigens, CD / Q000502:physiology; D002352:Carrier Proteins; D002448:Cell Adhesion; D002465:Cell Movement; D003598:Cytoskeletal Proteins / Q000502:physiology*; D022002:Hemidesmosomes / Q000502:physiology*; D006801:Humans; D051379:Mice; D008840:Microfilament Proteins / Q000502:physiology*; D018160:Receptors, Cytoplasmic and Nuclear / Q000502:physiology*; D060185:Tetraspanin 24; D015534:Trans-Activators; D014945:Wound Healing
D015703:Antigens, CD; C554715:CD151 protein, human; D002352:Carrier Proteins; C554716:Cd151 protein, mouse; D003598:Cytoskeletal Proteins; C098179:FLII protein, human; C000609263:FlII protein, mouse; D008840:Microfilament Proteins; D018160:Receptors, Cytoplasmic and Nuclear; D060185:Tetraspanin 24; D015534:Trans-Activators