Fig. 2.

Schematic representation of the proposed mechanism by which CK2 may contribute to accelerated degradation of CFTR. The F508 deletion makes Y512 more prone to phosphorylation by the Src family kinase Lyn [15]: this primes S511 phosphorylation by CK2, an event favoring CFTR degradation, which in turn generates fragments capable of stimulating CK2 activity [19] through a feed-back effect