Calcineurin, the calmodulin-dependent
serine/threonine phosphatase, is activated by elevations in intracellular
calcium leading to dephosphorylation of NFATc3
which enhances nuclear translocation. There, NFATc3 blocks
expression of the BK channel β1 subunit. Strong evidence
is provided that in diabetes mellitus, activation of calcineurin
dephosphorylates NFATc3, allowing it to move into the
nucleus, reduce transcription of the BK channel β1 subunit,
thereby decreasing calcium sensitivity of the BK channel