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. 2008 Jul 14;182(1):35–39. doi: 10.1083/jcb.200712124

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© 2008 Zhang and Sarge

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 3. — SUMO site K201R mutant lamin A and cardiomyopathy-associated E203G and E203K mutant lamin A proteins exhibit similar patterns of aberrant localization. (A and B) Wild-type, K201R, E203G, and E203K lamin A GFP fusion expression plasmids were transfected into HeLa cells (A) or mouse embryonic cardiomyocytes (B), and the subcellular localization of the GFP–lamin A proteins was examined by confocal fluorescence microscopy. DNA was visualized by staining with HOECHST 33342. Bars, 5 μm. (C) Wild-type, K201R, E203G, or E203K lamin A GFP fusion expression plasmids were transfected into HeLa cells, which were then analyzed by trypan blue assay to measure cell death. Data are shown as means ± SEM. (*, P < 0.0001; **, P < 0.0002; ***, P < 0.0001 [for lamin A mutants vs. wild type]) and are each from three datasets.