Inhibition of Ras-Induced Proliferation and Cellular Transformation by p16 INK4
- 13 January 1995
- journal article
- other
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 267 (5195) , 249-252
- https://doi.org/10.1126/science.7809631
Abstract
The cyclin-dependent kinase 4 (CDK4) regulates progression through the G 1 phase of the cell cycle. The activity of CDK4 is controlled by the opposing effects of the D-type cyclin, an activating subunit, and p16 INK4 , an inhibitory subunit. Ectopic expression of p16 INK4 blocked entry into S phase of the cell cycle induced by oncogenic Ha-Ras, and this block was relieved by coexpression of a catalytically inactive CDK4 mutant. Expression of p16 INK4 suppressed cellular transformation of primary rat embryo fibroblasts by oncogenic Ha-Ras and Myc, but not by Ha-Ras and E1a. Together, these observations provide direct evidence that p16 INK4 can inhibit cell growth.Keywords
This publication has 35 references indexed in Scilit:
- P16 gene in uncultured tumoursNature, 1994
- A Cell Cycle Regulator Potentially Involved in Genesis of Many Tumor TypesScience, 1994
- p21 is a universal inhibitor of cyclin kinasesNature, 1993
- A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4Nature, 1993
- Inhibition of cell proliferation by p107, a relative of the retinoblastoma protein.Genes & Development, 1993
- Integration of cell cycle control with transcriptional regulation by the retinoblastoma proteinCurrent Opinion in Cell Biology, 1993
- The SRF accessory protein Elk-1 contains a growth factor-regulated transcriptional activation domainCell, 1993
- For our eyes onlyNature, 1992
- Methylation-Sensitive Sequence-Specific DNA Binding by the c-Myc Basic RegionScience, 1991
- Translocation, breakage and truncated transcripts of c-myc oncogene in murine plasmacytomasNature, 1983