Expression of the myodystrophic R453W mutation of lamin A in C2C12 myoblasts causes promoter-specific and global epigenetic defects (Q39994086)

16 September 2017

Expression of the myodystrophic R453W mutation of lamin A in C2C12 myoblasts causes promoter-specific and global epigenetic defects (English)

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16 September 2017

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Anne-Mari Håkelien

1

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16 September 2017

Erwan Delbarre

2

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16 September 2017

Kristine G Gaustad

3

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16 September 2017

Brigitte Buendia

4

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16 September 2017

Philippe Collas

5

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16 September 2017

language of work or name

English

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publication date

7 March 2008

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Experimental Cell Research

16 September 2017

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16 September 2017

314

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16 September 2017

8

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16 September 2017

1869-1880

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Genetics of Laminopathies

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Expression of lamin A mutated in the carboxyl-terminal tail generates an aberrant nuclear phenotype similar to that observed in cells from patients with Dunnigan-type partial lipodystrophy and Emery-Dreifuss muscular dystrophy

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Expression of a mutant lamin A that causes Emery-Dreifuss muscular dystrophy inhibits in vitro differentiation of C2C12 myoblasts

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The dynamics of myogenin site-specific demethylation is strongly correlated with its expression and with muscle differentiation.

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Methyl CpG-binding proteins induce large-scale chromatin reorganization during terminal differentiation

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Stable CpG hypomethylation of adipogenic promoters in freshly isolated, cultured, and differentiated mesenchymal stem cells from adipose tissue

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X inactivation Xplained

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Nuclear lamin A inhibits adipocyte differentiation: implications for Dunnigan-type familial partial lipodystrophy

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Remodelling of the nuclear lamina and nucleoskeleton is required for skeletal muscle differentiation in vitro.

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10.1016/J.YEXCR.2008.02.018

7 January 2021

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DOI

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16 September 2017

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