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. 2014 Feb 20;10(2):e1004114. doi: 10.1371/journal.pgen.1004114

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© 2014 Banerjee et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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(A and B) Diagrammatic representation of (A) Wild Type and (B) Nesprin 1 and 2 double knockout cardiomyocyte nuclei. (A) Wild Type nuclei are anchored to the sarcomeric structure via Nesprin 1 and 2. Application of 14% anisotropic loading results in normal cellular biomechanical gene response (egr-1, c-jun, iex-1, c-fos and c-myc.). Cardiac development and nuclear positioning/morphology are also normal in these cells. (B) Loss of both Nesprin 1 and 2 causes ablation of biomechanical gene response upon application of strain. Hearts from these mice develop cardiomyopathy with fibrosis, and have altered nuclear positioning and morphology.