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Myocyte stress 1 plays an important role in cellular hypertrophy and protection against apoptosis

By A.L. Koekemoer, N.W. Chong, A.H. Goodall and N.J. Samani

Abstract

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: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

Topics: MS1, Hypertrophy, Apoptosis, NOL3, MRTF, SRF, STARS
Publisher: Elsevier
Year: 2009
DOI identifier: 10.1016/j.febslet.2009.08.011
OAI identifier: oai:lra.le.ac.uk:2381/7870
Journal:

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  1. (2007). Bcl-2 family members and apoptosis, taken to heart. doi
  2. (1998). ARC, an inhibitor of apoptosis expressed in skeletal muscle and heart that interacts selectively with caspases. doi
  3. (2003). Apoptosis repressor with caspase domain inhibits cardiomyocyte apoptosis by reducing K+ currents. doi
  4. (2007). Modulation of adverse cardiac remodeling by STARS, a mediator of MEF2 signaling and SRF activity. doi
  5. (2009). Regulation of STARS and its downstream targets suggest a novel pathway involved in human skeletal muscle hypertrophy and atrophy. doi
  6. (2003). Megakaryoblastic leukemia 1, a potent transcriptional coactivator for serum response factor (SRF), is required for serum induction of SRF target genes. doi
  7. (1986). Upstream regions of the human cardiac actin gene that modulate its transcription in muscle cells: presence of an evolutionarily conserved repeated motif. doi
  8. (1987). Duplicated CArG box domains have positive and mutually dependent regulatory roles in expression of the human alpha-cardiac actin gene. doi
  9. (2003). Serum response factor: toggling between disparate programs of gene expression. doi
  10. (2005). Mitogen regulated induction of FRA-1 proto-oncogene is controlled by the transcription factors binding to both serum and TPA response elements. doi
  11. (2006). Defining the mammalian CArGome.
  12. (2005). SRF-dependent gene expression in isolated cardiomyocytes: Regulation of genes involved in cardiac hypertrophy. doi
  13. (1999). ARC inhibits cytochrome c release from mitochondria and protects against hypoxia-induced apoptosis in heart-derived H9c2 cells. doi
  14. (2001). The apoptotic regulatory protein ARC (apoptosis repressor with caspase recruitment domain) prevents oxidant stress-mediated cell death by preserving mitochondrial function. doi
  15. (2002). TAT protein transduction into isolated perfused hearts: TAT-apoptosis repressor with caspase recruitment domain is cardioprotective. doi
  16. (1991). A rapid and simple method for measuring thymocyte apoptosis by propidium iodide staining and flow cytometry. doi
  17. (1991). Evaluation of glucocorticoidinduced DNA fragmentation in mouse thymocytes by flow cytometry. doi
  18. (1992). Comparative evaluation of several DNA binding dyes in the detection of apoptosis-associated chromatin degradation by flow cytometry. doi

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