期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 97, 期 5, 页码 2229-2234出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.050586197
关键词
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资金
- NCI NIH HHS [R37 CA057345, R01 CA057341, CA57341, R01 CA057345, CA-57345] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007601, R01 GM041690, GM-41690] Funding Source: Medline
The prototypic oncogene c-MYC encodes a transcription factor that can drive proliferation by promoting cell-cycle reentry. However, the mechanisms through which c-MYC achieves these effects have been unclear. Using serial analysis of gene expression, we have identified the cyclin-dependent kinase 4 (CDK4) gene as a transcriptional target of c-MYC, c-MYC induced a rapid increase in CDK4 mRNA levels through four highly conserved c-MYC binding sites within the CDK4 promoter. Cell-cycle progression is delayed in c-MYC-deficient RAT1 cells, and this delay was associated with a defect in CDK4 induction. Ectopic expression of CDK4 in these cells partially alleviated the growth defect. Thus, CDK4 provides a direct link between the oncogenic effects of c-MYC and cell-cycle regulation.
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