Fig. 2

Schematic representation of the role of CK2 on ER stress response. CK2 promotes a compensatory UPR by stabilizing IRE1α, inhibiting the kinase PERK and, consequently, the phosphorylation of Ser51 (S51) on EIF2α. Moreover, CK2, by phosphorylating Ser13 (S13) of Cdc37, tightens its association with chaperones, leading to MM plasma cell survival, proliferation, and enhanced stress-coping ability. CK2 inactivation (chemically or with gene silencing) leads to a deregulation of the above cascades, inducing MM cell apoptosis