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Fig. 7. Model of the mechanism by which calmodulin (CaM) regulates polycystic kidney disease 2-like-1 (PKD2L1). (A) In 16 nM free calcium (blue), EF-hand (yellow) constantly binds to channel and shows weak inhibition. CaM C-lobe (green) is bound to PKD2L1 through Leu-593, a CaM C-lobe anchor residue (upper panel). At this time, if EF-hand deletion occurs, PKD2L1 inhibition by EF-hand is weakened (lower panel). (B) When calcium increases to 100 nM, CaM N-lobe (orange) binds to PKD2L1 instead of EF-hand, resulting in strong PKD2L1 inhibition (upper panel). Even with EF-hand deletion, CaM N-lobe still binds to PKD2L1 and strongly inhibits its activity (lower panel). The thick line indicates strong action.
Korean J Physiol Pharmacol 2020;24:277-286
© Korean J Physiol Pharmacol