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| mice lacking HDAC2 survive until the perinatal period, when they succumb to a spectrum of cardiac defects with obliteration of the lumen of the right ventricle, excessive hyperplasia and apoptosis of cardiomyocytes, and bradycardia  | |
Cardiac-specific deletion of HDAC1 and HDAC2 genes results in neonatal lethality with cardiac arrhythmias, dilated cardiomyopathy, and up-regulation of genes encoding skeletal muscle-specific contractile proteins and calcium channels |
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deletion of both HDAC1 and HDAC2 genes in mouse developing neurons results in severe hippocampal abnormalities, absence of cerebellar foliation, disorganization of cortical neurons, and lethality by postnatal day 7 |
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loss of HDAC2 in NFe2l2 deficient mice is a crucial component of increased susceptibility to oxidative stress-induced inflammatory response in the lungs |
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ablation of Hdac1 and Hdac2 specifically in mouse Schwann cells, result in massive Schwann cell loss and virtual absence of myelin in mutant sciatic nerves ( |