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BMI-1026 treatment can induce SAHF formation by activation of Erk1/2

  • Seo, Hyun-Joo (Department of Biochemistry, College of Medicine, Dankook University) ;
  • Park, Hye-Jeong (Department of Biochemistry, College of Medicine, Dankook University) ;
  • Choi, Hyung-Su (Department of Biochemistry, College of Medicine, Dankook University) ;
  • Hwang, So-Yoon (Department of Biochemistry, College of Medicine, Dankook University) ;
  • Park, Jeong-Soo (Department of Biochemistry, College of Medicine, Dankook University) ;
  • Seong, Yeon-Sun (Department of Biochemistry, College of Medicine, Dankook University)
  • Published : 2008.07.31

Abstract

BMI-1026 is a synthetic aminopyrimidine compound that targets cyclin dependent kinases (cdks) and was initially designed as a potential anticancer drug. Even though it has been well documented that BMI-1026 is a potent cdk inhibitor, little is known about the cellular effects of this compound. In this study, we examined the effects of BMI-1026 treatment on inducing premature senescence and then evaluated the biochemical features of BMI-1026-induced premature senescence. From these experiments we determined that BMI-1026 treatment produced several biochemical features of premature senescence and also stimulated expression of mitogen activated protein kinase (MAPK) family proteins. BMI-1026 treatment caused nuclear translocation of activated Erk1/2 and the formation of senescence associated heterochromatin foci in 5 days. The heterochromatin foci formation was perturbed by inhibition of Erk1/2 activation.

Keywords

References

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