Publication Date:
1996-05-10
Description:
Cells deprived of serum mitogens will either undergo immediate cell cycle arrest or complete mitosis and arrest in the next cell cycle. The transition from mitogen dependence to mitogen independence occurs in the mid-to late G1 phase of the cell cycle and is called the restriction point. Murine Balb/c-3T3 fibroblasts deprived of serum mitogens accumulated the cyclin-dependent kinase (CDK) inhibitor p27Kip1. This was correlated with inactivation of essential G1 cyclin-CDK complexes and with cell cycle arrest in G1. The ability of specific mitogens to allow transit through the restriction point paralleled their ability to down-regulate p27, and antisense inhibition of p27 expression prevented cell cycle arrest in response to mitogen depletion. Therefore, p27 is an essential component of the pathway that connects mitogenic signals to the cell cycle at the restriction point.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coats, S -- Flanagan, W M -- Nourse, J -- Roberts, J M -- New York, N.Y. -- Science. 1996 May 10;272(5263):877-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8629023" target="_blank"〉PubMed〈/a〉
Keywords:
3T3 Cells
;
Amino Acid Sequence
;
Animals
;
Base Sequence
;
*Cell Cycle Proteins
;
Culture Media
;
Cyclin-Dependent Kinase Inhibitor p27
;
Cyclin-Dependent Kinases/*antagonists & inhibitors/metabolism
;
Cyclins/metabolism
;
Down-Regulation
;
Enzyme Inhibitors/*metabolism
;
Epidermal Growth Factor/pharmacology
;
*G1 Phase
;
Gene Expression/drug effects
;
Insulin-Like Growth Factor I/pharmacology
;
Mice
;
Microtubule-Associated Proteins/biosynthesis/genetics/*metabolism
;
Mitogens/pharmacology
;
Molecular Sequence Data
;
Oligonucleotides, Antisense/pharmacology
;
Platelet-Derived Growth Factor/pharmacology
;
Proto-Oncogene Proteins c-sis
;
*Tumor Suppressor Proteins
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
