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Transgenic overexpression of Hdac3 in the heart produces increased postnatal cardiac myocyte proliferation but does not induce hypertrophy.
Hopx and Hdac2 interact to modulate Gata4 acetylation and embryonic cardiac myocyte proliferation.
Homeodomain only protein x is down-regulated in human heart failure.
Acetylation of a conserved lysine residue in the ATP binding pocket of p38 augments its kinase activity during hypertrophy of cardiomyocytes.
Targeted deletion of Tsc1 causes fatal cardiomyocyte hyperplasia independently of afterload.