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Heregulin-induced epigenetic regulation of the utrophin-A promoter.


ABSTRACT: Utrophin is the autosomal homolog of dystrophin, the product of the Duchenne's muscular dystrophy (DMD) locus. Utrophin is of therapeutic interest since its over-expression can compensate dystrophin's absence. Utrophin is enriched at neuromuscular junctions due to heregulin-mediated utrophin-A promoter activation. We demonstrate that heregulin activated MSK1/2 and phosphorylated histone H3 at serine 10 in cultured C2C12 muscle cells, in an ERK-dependent manner. MSK1/2 inhibition suppressed heregulin-mediated utrophin-A activation. MSK1 over-expression potentiated heregulin-mediated utrophin-A activation and chromatin remodeling at the utrophin-A promoter. These results identify MSK1/2 as key effectors modulating utrophin-A expression as well as identify novel targets for DMD therapy.

SUBMITTER: Basu U 

PROVIDER: S-EPMC2699486 | biostudies-literature | 2007 Sep

REPOSITORIES: biostudies-literature

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Heregulin-induced epigenetic regulation of the utrophin-A promoter.

Basu Utpal U   Gyrd-Hansen Mads M   Baby Santhosh M SM   Lozynska Olga O   Krag Thomas O B TO   Jensen Claus J CJ   Frödin Morten M   Khurana Tejvir S TS  

FEBS letters 20070723 22


Utrophin is the autosomal homolog of dystrophin, the product of the Duchenne's muscular dystrophy (DMD) locus. Utrophin is of therapeutic interest since its over-expression can compensate dystrophin's absence. Utrophin is enriched at neuromuscular junctions due to heregulin-mediated utrophin-A promoter activation. We demonstrate that heregulin activated MSK1/2 and phosphorylated histone H3 at serine 10 in cultured C2C12 muscle cells, in an ERK-dependent manner. MSK1/2 inhibition suppressed hereg  ...[more]

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