Calcineurin regulates an electrophysiological mechanism that activates the transcription of specific developmental genes in a heirarchical manner to scale fish appendages.

Longevity in C. elegans is influenced not only by insulin/IGF-1 signalling, but also by CAMKII and calcineurin, acting on the same target, the transcription factor DAF-16.

The ability of calcium waves to exert different effects on calcineurin activity depending on subcellular location is mediated by the distribution of calmodulin.

Calcineurin inhibition has opposing effects on Caenorhabditis elegans lifespan and survival on pathogens via its role in the defecation motor program.

Calcium overload in cardiomyocytes disrupts sarcomere integrity, by stimulating transcriptional upregulation of the E3 ubiquitin ligase MuRF1.

In vivo imaging reveals that gradually increased amount of glucose mediates the heterogeneous functional development of individual β-cells by activating its major downstream calcineurin/NFAT signaling pathway.

Discovery of a non-canonical mechanism for decreasing protein kinase A activity that does not require lowering of cyclic AMP.

Global transcriptome changes, particularly alternative splicing, are highly dynamic the first 2 weeks after birth, and the example of calcineurin A splicing exemplifies the importance of alternative splicing during skeletal muscle development.

The target-myristoyl switch induced by protein-protein interaction is a novel regulatory mechanism for myristoylated EF-hand calcium-binding proteins, in which target binding facilitates exposure of the myristoyl anchor and the association to the lipid membrane in a calcium-independent manner.

A novel high-throughput method for measuring many weak protein-peptide affinities simultaneously reveals how calcineurin, a human phosphatase essential for the immune response, recognizes its peptide substrates.