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10.1038/ncomms7138 http://scihub22266oqcxt.onion/10.1038/ncomms7138 C4304400!4304400!25609380     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2015 ; 6 (ä): 6138 Nephropedia Template TP {{tp|p=25609380|t=2015. Chromatin De-Compaction By The Nucleosomal Binding Protein HMGN5 Impairs Nuclear Sturdiness |pdf=|usr=}}{{25609380}} gab.com Text Chromatin De-Compaction By The Nucleosomal Binding Protein HMGN5 Impairs Nuclear Sturdiness JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25609380 #FOAvip In most metazoan nuclei, heterochromatin is located at the nuclear periphery in contact with the nuclear lamina, which provides mechanical stability to the nucleus. We show that in cultured cells, chromatin de-compaction by the nucleosome binding protein HMGN5 decreases the sturdiness, elasticity, and rigidity of the nucleus. Mice overexpressing HMGN5, either globally or only in the heart, are normal at birth but develop hypertrophic heart with large cardiomyoctyes, deformed nuclei and disrupted lamina, and die of cardiac malfunction. Chromatin de-compaction is seen in cardiomyocytes of newborn mice but misshaped nuclei with disrupted lamina are seen only in adult cardiomyocytes, suggesting that loss of heterochromatin diminishes the ability of the nucleus to withstand the mechanical forces of the contracting heart. Thus, heterochromatin enhances the ability of the nuclear lamina to maintain the sturdiness and shape of the eukaryotic nucleus; a structural role for chromatin that is distinct from its genetic functions. Twit Text FOAVip Chromatin De-Compaction By The Nucleosomal Binding Protein HMGN5 Impairs Nuclear Sturdiness ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25609380 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25609380 #FOAvip English Wikipedia <ref>{{Cite pmid|25609380}}</ref> Chromatin De-Compaction By The Nucleosomal Binding Protein HMGN5 Impairs Nuclear Sturdiness #MMPMID25609380 Furusawa T; Rochman M; Taher L; Dimitriadis EK; Nagashima K; Anderson S; Bustin M Nat Commun 2015[]; 6 (ä): 6138 PMID25609380show ga In most metazoan nuclei, heterochromatin is located at the nuclear periphery in contact with the nuclear lamina, which provides mechanical stability to the nucleus. We show that in cultured cells, chromatin de-compaction by the nucleosome binding protein HMGN5 decreases the sturdiness, elasticity, and rigidity of the nucleus. Mice overexpressing HMGN5, either globally or only in the heart, are normal at birth but develop hypertrophic heart with large cardiomyoctyes, deformed nuclei and disrupted lamina, and die of cardiac malfunction. Chromatin de-compaction is seen in cardiomyocytes of newborn mice but misshaped nuclei with disrupted lamina are seen only in adult cardiomyocytes, suggesting that loss of heterochromatin diminishes the ability of the nucleus to withstand the mechanical forces of the contracting heart. Thus, heterochromatin enhances the ability of the nuclear lamina to maintain the sturdiness and shape of the eukaryotic nucleus; a structural role for chromatin that is distinct from its genetic functions. äChromatin De-Compaction By The Nucleosomal Binding Protein HMGN5 Impai(epmc).pdf DeepDyve Pubget Overpricing