Publication Date:
1995-01-13
Description:
The cyclin-dependent kinase 4 (CDK4) regulates progression through the G1 phase of the cell cycle. The activity of CDK4 is controlled by the opposing effects of the D-type cyclin, an activating subunit, and p16INK4, an inhibitory subunit. Ectopic expression of p16INK4 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 p16INK4 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 p16INK4 can inhibit cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Serrano, M -- Gomez-Lahoz, E -- DePinho, R A -- Beach, D -- Bar-Sagi, D -- CA55360/CA/NCI NIH HHS/ -- EY09300-01/EY/NEI NIH HHS/ -- HD28317-02/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1995 Jan 13;267(5195):249-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, NY 11724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7809631" target="_blank"〉PubMed〈/a〉
Keywords:
Adenovirus E1A Proteins/genetics/physiology
;
Animals
;
Carrier Proteins/genetics/*physiology
;
*Cell Division
;
*Cell Transformation, Neoplastic
;
Cells, Cultured
;
Cyclin-Dependent Kinase 4
;
Cyclin-Dependent Kinase Inhibitor p16
;
*Cyclin-Dependent Kinases
;
Genes, Reporter
;
Genes, Retinoblastoma
;
Genes, myc
;
Genes, ras
;
Plasmids
;
Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism
;
*Proto-Oncogene Proteins
;
Rats
;
Retinoblastoma Protein/physiology
;
S Phase
;
Transcriptional Activation
;
Transfection
;
Tumor Cells, Cultured
;
ras Proteins/genetics/*physiology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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