Abstract
Dynamin 2 (DNM2) is involved in endocytosis and intracellular membrane trafficking through its function in vesicle formation from distinct membrane compartments. During the last decade, several studies pointed out an important role of DNM2-dependent trafficking in turnover of focal adhesions which represent a physical link between the extracellular matrix and the intracellular actin cytoskeleton, and a platform for several signalling pathways. Here, we review the involvement of DNM2 in structural and functional aspects of the focal adhesion sites. Mutations in the DNM2 gene cause two hereditary neuromuscular disorders: dominant centronuclear myopathy and Charcot-Marie-Tooth peripheral neuropathy. Potential impairment of focal adhesions as a pathophysiological hypothesis in DNM2-related human diseases is discussed.
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