Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/7870
Title: Myocyte stress 1 plays an important role in cellular hypertrophy and protection against apoptosis
Authors: Koekemoer, A.L.
Chong, N.W.
Goodall, A.H.
Samani, N.J.
First Published: Sep-2009
Publisher: Elsevier
Citation: FEBS Letters 583 (2009) 2964-2967. Myocyte stress 1 plays an important role in cellular hypertrophy and protection against apoptosis. Andrea L. Koekemoer, Nelson W. Chong, Alison H. Goodall, Nilesh J. Samani
Abstract: Myocyte stress 1 (MS1) is a recently described striated muscle actin-binding protein that is up-regulated in the early stages of pressure overload left ventricular hypertrophy. The aim of this study was to determine whether MS1 induces cellular hypertrophy and protects against apoptosis. Over-expressed MS1 co-localized with actin in H9c2 cells and altered expression of genes of the myocardin-related transcription factor (MRTF)/serum response factor (SRF) transcriptional pathways and in addition the apoptosis repressor with caspase recruitment domain (Nol3) gene. The size of cells over-expressing MS1 was significantly increased by 55% and over-expression of MS1 dramatically inhibited staurosporine-induced apoptosis by 89%. These findings suggest the involvement of MS1 in cellular hypertrophy and protection against apoptosis.
ISSN: 0014-5793
Links: http://dx.doi.org/10.1016/j.febslet.2009.08.011
http://hdl.handle.net/2381/7870
Type: Article
Description: This is the author’s final draft post-refereeing of FEBS Letters 583 (2009) 2964-2967. Myocyte stress 1 plays an important role in cellular hypertrophy and protection against apoptosis. Andrea L. Koekemoer, Nelson W. Chong, Alison H. Goodall, Nilesh J. Samani. The final published version is available at the DOI below:
Appears in Collections:Published Articles, Dept. of Cardiovascular Sciences

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ms1_paper_FEBS_text_300709 final.pdf91.54 kBAdobe PDFView/Open
Supplementary Table 1.pdf76.67 kBAdobe PDFView/Open
Supplementary data_300709 final.pdf97.39 kBAdobe PDFView/Open
figure 1.pdf22.45 kBAdobe PDFView/Open
figure 2.pdf4.31 kBAdobe PDFView/Open
figure 3.pdf6.54 kBAdobe PDFView/Open


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