|Regulation of the cell cycle in response to inhibition of mitochondrial generated energy.|
|PMID: 15925326 Owner: NLM Status: MEDLINE|
|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 of oligomycin result in a cell cycle arrest of HL-60 cells in G(1) [S. Sweet, G. Singh, Accumulation of human promyelocytic leukemic (HL-60) cells at two energetic cell cycle checkpoints, Cancer Res. 55 (1995) 5164-5167]. In this study, we provide the molecular mechanisms for the observed G(1) arrest following mitochondrial ATPase inhibition. Protein expression of cyclin E and CDK2, the kinase activity of complexed cyclin E/CDK2, and protein expression of p16, p21, and p27 were all unaffected by oligomycin administration. While CDK4 levels were unchanged following oligomycin treatment, a dramatic reduction in cyclin D(1) was observed. Moreover, increased amounts of hypo-phosphorylated retinoblastoma protein (Rbp) and Rbp bound E2F were observed following mitochondrial ATP synthase inhibition. These data provide further evidence that surveillance of available energy occurs during G(1) and ATP deprivation results in cell cycle arrest via a reduction in cyclin D.|
|Adam Gemin; Susan Sweet; Tom J Preston; Gurmit Singh|
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|Type: Journal Article; Research Support, Non-U.S. Gov't|
|Title: Biochemical and biophysical research communications Volume: 332 ISSN: 0006-291X ISO Abbreviation: Biochem. Biophys. Res. Commun. Publication Date: 2005 Jul|
|Created Date: 2005-06-13 Completed Date: 2005-08-04 Revised Date: 2012-06-25|
Medline Journal Info:
|Nlm Unique ID: 0372516 Medline TA: Biochem Biophys Res Commun Country: United States|
|Languages: eng Pagination: 1122-32 Citation Subset: IM|
|Juravinski Cancer Centre, 699 Concession St., Hamilton, Ont., Canada L8V 5C2.|
|APA/MLA Format Download EndNote Download BibTex|
CDC2-CDC28 Kinases / biosynthesis
Cell Cycle Proteins / biosynthesis, metabolism
Cyclin D1 / metabolism
Cyclin E / biosynthesis
Cyclin-Dependent Kinase 2
Cyclin-Dependent Kinase Inhibitor p16 / biosynthesis
Cyclin-Dependent Kinase Inhibitor p21
Cyclin-Dependent Kinase Inhibitor p27
Cyclin-Dependent Kinases / metabolism
Cyclins / metabolism
DNA / chemistry
DNA-Binding Proteins / metabolism
E2F Transcription Factors
Mitochondria / metabolism*
Mitochondrial Proton-Translocating ATPases / metabolism
Oligomycins / chemistry
Retinoblastoma Protein / metabolism
Transcription Factors / metabolism
Tumor Suppressor Proteins / biosynthesis
|0/CDKN1A protein, human; 0/Cell Cycle Proteins; 0/Cyclin D; 0/Cyclin E; 0/Cyclin-Dependent Kinase Inhibitor p16; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Cyclins; 0/DNA-Binding Proteins; 0/E2F Transcription Factors; 0/Oligomycins; 0/Retinoblastoma Protein; 0/Transcription Factors; 0/Tumor Suppressor Proteins; 136601-57-5/Cyclin D1; 147604-94-2/Cyclin-Dependent Kinase Inhibitor p27; 56-65-5/Adenosine Triphosphate; 9007-49-2/DNA; EC 220.127.116.11/CDC2-CDC28 Kinases; EC 18.104.22.168/CDK2 protein, human; EC 22.214.171.124/Cyclin-Dependent Kinase 2; EC 126.96.36.199/Cyclin-Dependent Kinases; EC 3.6.3.-/Mitochondrial Proton-Translocating ATPases|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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