Abstract
Fyn, a member of the Src family kinases (SFKs), has been shown to play important yet contradictory roles in keratinocyte (KC) adhesion. During KC differentiation, physiological activation of Fyn results in the formation of adherens junctions, recruiting junctional components and inducing signaling pathways that control the differentiation program. However, in KC transformation and oncogenesis, increased Fyn activity has been implicated in the dissolution of adhesion structures and an increased migratory phenotype. Fyn activity is also associated with both the formation and dissolution of focal adhesions, and to a lesser extent hemidesmosomes and desmosomes. This viewpoint article aims to reconcile these disparate bodies of literature regarding Fyn's role in cell-cell and cell-matrix adhesion by proposing several alternative, testable hypotheses that unify Fyn's fractured functions.
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