Key result
Cardiac-specific deletion of MED12 in mice leads to progressive dilated cardiomyopathy by disrupting the transcriptional network of calcium-handling genes and altering calcium cycling.
Population
Mice with conditional cardiac-specific deletion of MED12 and littermate controls, as well as isolated…
Comparison
Cardiac-specific deletion of Med12 vs Littermate controls (αMhc-Cre–Med12fl/y)
Design
Preclinical
Follow-up
up to 12 weeks of age
Authors
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Does not alter clinical management; leaves open MED12 as a transcriptional target in human dilated cardiomyopathy.
MED12 is a critical transcriptional regulator of calcium-handling genes in the heart, and its loss leads to early-onset dilated cardiomyopathy.
Baskin et al. (2017) studied Dilated cardiomyopathy. Cardiac-specific deletion of Med12 vs. Wild-type / control mice was evaluated on Cardiac function and calcium-handling gene expression. Cardiac-specific deletion of MED12 in mice leads to progressive dilated cardiomyopathy by disrupting the transcriptional network of calcium-handling genes and altering calcium cycling.
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