Fig. 3

The DCTN1-ALK intra-chromosomal rearrangement detected in this case conformed to the common structural organization of ALK fusions, with the vast majority having an ALK intron 19 breakpoint and is a priori suspected to active in vivo. The DCTN1 component of the fusion contains exons including the coiled-coil domains, which is similar to other previously reported ALK fusion partners. Via these domains, DCTN1 is suspected to promote dimerization of ALK and subsequent kinase activation by transphosphorylation