ROLE OF GDAP2 IN INTEGRATING ERK-FAK SIGNALING FOR CELL MIGRATION AND CANCER METASTASIS

Abstract

Cell migration is a crucial phenomenon regulating various normal physiological processes and pathological conditions. This process requires interplay of various signaling pathways that regulate cell adhesion, cell spreading, morphogenesis and motility. One such key regulator is the membrane-bound Focal Adhesion Kinase (FAK). It was observed that phosphorylation of FAK via ERK pathway influences migration. However, the exact mechanism that integrates ERK and FAK signaling is not well understood. In this study we elucidate how GDAP2 (Ganglioside- induced Differentiation-Associated-Protein 2), a BCH domain containing protein, is critical for regulating ERK dependent FAK function and controlling cell migration.