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

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Heregulin-induced epigenetic regulation of the utrophin-A promoter. / Basu, Utpal; Gyrd-Hansen, Mads; Baby, Santhosh M; Lozynska, Olga; Krag, Thomas O B; Jensen, Claus J; Frödin, Morten; Khurana, Tejvir S.

In: FEBS Letters, Vol. 581, No. 22, 2007, p. 4153-8.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Basu, U, Gyrd-Hansen, M, Baby, SM, Lozynska, O, Krag, TOB, Jensen, CJ, Frödin, M & Khurana, TS 2007, 'Heregulin-induced epigenetic regulation of the utrophin-A promoter.', FEBS Letters, vol. 581, no. 22, pp. 4153-8. https://doi.org/10.1016/j.febslet.2007.07.021

APA

Basu, U., Gyrd-Hansen, M., Baby, S. M., Lozynska, O., Krag, T. O. B., Jensen, C. J., Frödin, M., & Khurana, T. S. (2007). Heregulin-induced epigenetic regulation of the utrophin-A promoter. FEBS Letters, 581(22), 4153-8. https://doi.org/10.1016/j.febslet.2007.07.021

Vancouver

Basu U, Gyrd-Hansen M, Baby SM, Lozynska O, Krag TOB, Jensen CJ et al. Heregulin-induced epigenetic regulation of the utrophin-A promoter. FEBS Letters. 2007;581(22):4153-8. https://doi.org/10.1016/j.febslet.2007.07.021

Author

Basu, Utpal ; Gyrd-Hansen, Mads ; Baby, Santhosh M ; Lozynska, Olga ; Krag, Thomas O B ; Jensen, Claus J ; Frödin, Morten ; Khurana, Tejvir S. / Heregulin-induced epigenetic regulation of the utrophin-A promoter. In: FEBS Letters. 2007 ; Vol. 581, No. 22. pp. 4153-8.

Bibtex

@article{a3916070224e11ddbc23000ea68e967b,
title = "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.",
author = "Utpal Basu and Mads Gyrd-Hansen and Baby, {Santhosh M} and Olga Lozynska and Krag, {Thomas O B} and Jensen, {Claus J} and Morten Fr{\"o}din and Khurana, {Tejvir S}",
note = "Keywords: Animals; Cells, Cultured; Chromatin Assembly and Disassembly; Enzyme Activation; Epigenesis, Genetic; Histones; Mice; Models, Genetic; Muscle Cells; Neuregulin-1; Phosphorylation; Promoter Regions (Genetics); Ribosomal Protein S6 Kinases, 90-kDa; Utrophin",
year = "2007",
doi = "10.1016/j.febslet.2007.07.021",
language = "English",
volume = "581",
pages = "4153--8",
journal = "F E B S Letters",
issn = "0014-5793",
publisher = "JohnWiley & Sons Ltd",
number = "22",

}

RIS

TY - JOUR

T1 - Heregulin-induced epigenetic regulation of the utrophin-A promoter.

AU - Basu, Utpal

AU - Gyrd-Hansen, Mads

AU - Baby, Santhosh M

AU - Lozynska, Olga

AU - Krag, Thomas O B

AU - Jensen, Claus J

AU - Frödin, Morten

AU - Khurana, Tejvir S

N1 - Keywords: Animals; Cells, Cultured; Chromatin Assembly and Disassembly; Enzyme Activation; Epigenesis, Genetic; Histones; Mice; Models, Genetic; Muscle Cells; Neuregulin-1; Phosphorylation; Promoter Regions (Genetics); Ribosomal Protein S6 Kinases, 90-kDa; Utrophin

PY - 2007

Y1 - 2007

N2 - 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.

AB - 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.

U2 - 10.1016/j.febslet.2007.07.021

DO - 10.1016/j.febslet.2007.07.021

M3 - Journal article

C2 - 17692845

VL - 581

SP - 4153

EP - 4158

JO - F E B S Letters

JF - F E B S Letters

SN - 0014-5793

IS - 22

ER -

ID: 4076009