(A) Domains of calcineurin.
The importance of calcineurin in mitochondrial fission was further investigated by RNAi studies.
We then attempted to explore the mechanism underlying the proteolytic activation of calcineurin.
For example, the association of calcineurin inhibitor use and AKI may reflect the association of AKI with transplant status.
The importance of calcineurin in mitochondrial fission is also supported by the findings that an inhibitor of calcineurin (Cereghetti et al., 2010) or the use of a miRNA targeting calcineurin (Wang et al., 2011) regulates mitochondrial fission by modulating Drp1 dephosphorylation and translocation.
Calcineurin is high in developing striosomes [83] therefore decreased striosomal pCREB [84] and increased Nr4a1-eGFP may result through the same pathway, activity-dependent activation of calcineurin.
To examine calcineurin-dependent pathways, we utilized FK506 (Tacrolimus), an immunosuppressive molecule that inhibits calcineurin, as well as drugs that inhibit cyclophilin A-mediated activation of calcineurin.
NFATc is not only dephosphorylated by calcineurin but additionally interacts with calcineurin via two motifs binding at regions distinct from the catalytic centre of calcineurin.
Inhibition of calcineurin totally blocks the adaptive immune response.
Notably, this phenotype can be rescued by overactivation of calcineurin.
