Regulation of the cell cycle in response to inhibition of mitochondrial generated energy.
作者： Adam Gemin , Susan Sweet , Tom J. Preston , Gurmit Singh
DOI: 10.1016/J.BBRC.2005.05.061
关键词:
摘要: Abstract Cell cycle control is regulated through the temporal action of both cyclin-dependent kinases and cyclin binding partners. Previously, we have demonstrated that low doses oligomycin result in a cell arrest HL-60 cells G1 [S. Sweet, G. Singh, Accumulation human promyelocytic leukemic (HL-60) at two energetic checkpoints, Cancer Res. 55 (1995) 5164–5167]. In this study, provide molecular mechanisms for observed following mitochondrial ATPase inhibition. Protein expression E CDK2, kinase activity complexed E/CDK2, protein p16, p21, p27 were all unaffected by administration. While CDK4 levels unchanged treatment, dramatic reduction D1 was observed. Moreover, increased amounts hypo-phosphorylated retinoblastoma (Rbp) Rbp bound E2F ATP synthase These data further evidence surveillance available energy occurs during deprivation results via D.
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