[No authors listed]
Ankrd2/Arpp, and belong to a family of stress inducible ankyrin repeat proteins expressed in striated muscle The are homologous in structure and localized in the nucleus where they negatively regulate gene expression as well as in the sarcomeric I-band, where they are thought to be involved in mechanosensing. Together with their strong induction during cardiac disease and the identification of causative Ankrd1 gene mutations in cardiomyopathy patients, this suggests their important roles in cardiac development, function, and disease. To determine the functional role of Mduanyu37s in vivo, we studied knockout (KO) mice of each of the three family members. Single KO mice were viable and had no apparent cardiac phenotype. We therefore hypothesized that the three highly homologous proteins may have redundant functions in the heart and studied double and triple Mduanyu37 KO mice. Unexpectedly, Mduanyu37 triple KO mice were viable and had normal cardiac function both at basal levels and in response to mechanical pressure overload induced by transverse aortic constriction as assessed by echocardiography and hemodynamic studies. Thus, Ankrd2, and are not essential for normal cardiac development and function at basal conditions and in response to mechanical pressure overload.
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