Document Detail

Cyclins and CDKS in development and cancer: lessons from genetically modified mice.
MedLine Citation:
PMID:  16146805     Owner:  NLM     Status:  MEDLINE    
From yeast to humans, cell cycle progression and cell division are driven by the sequential activation of a group of serine-threonine kinases called cyclin-dependent kinases (Cdks). Multiple Cdks control the cell cycle in mammals and have been long considered essential for normal proliferation, development and homeostasis. The importance of the Cdk-cyclin complexes in cell proliferation is underscored by the finding that deregulation of the Cdk activity is found in virtually the whole spectrum of human tumors. Recent information from gene-targeted mouse models for the various cyclins and Cdks have made some of the generally accepted concepts of cell cycle regulation to be revised and new and exciting questions to be investigated. Unexpectedly, most of the canonical Cdk-cyclin complexes have turned out to be dispensable for cell proliferation due to a high level of functional redundancy, promiscuity and compensatory mechanisms. As a consequence, a "yeast-like" model where only one Cdk is essential to drive all stages of cell cycle progression is starting to be envisioned for mammalian cells. Moreover, the specific molecular players that drive the cell cycle in mammals seem to be cell-type-specific, and new, non-canonical functions of cyclins and Cdks have been revealed. This review will discuss these new findings and their implications for cancer therapy.
David Santamaria; Sagrario Ortega
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2006-01-01
Journal Detail:
Title:  Frontiers in bioscience : a journal and virtual library     Volume:  11     ISSN:  1093-4715     ISO Abbreviation:  Front. Biosci.     Publication Date:  2006  
Date Detail:
Created Date:  2005-09-08     Completed Date:  2006-06-02     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9709506     Medline TA:  Front Biosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1164-88     Citation Subset:  IM    
Molecular Oncology Program, Spanish National Cancer Centre (CNIO), 28029-Madrid, Spain.
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MeSH Terms
Cell Cycle
Cell Division
Cell Line
Cell Proliferation
Cell Transformation, Neoplastic
Cyclin D
Cyclin E / metabolism
Cyclin-Dependent Kinase 2 / metabolism
Cyclin-Dependent Kinase 4 / metabolism
Cyclin-Dependent Kinase 6 / metabolism
Cyclin-Dependent Kinase Inhibitor Proteins / metabolism
Cyclin-Dependent Kinase Inhibitor p21 / metabolism
Cyclin-Dependent Kinase Inhibitor p27 / metabolism
Cyclin-Dependent Kinases / metabolism*
Cyclins / metabolism,  physiology*
G1 Phase
G2 Phase
Genes, Tumor Suppressor
Immunity, Innate
Mice, Transgenic
Models, Biological
Models, Genetic
Neoplasms / metabolism*
Placenta / metabolism
Point Mutation
Retinoblastoma Protein / metabolism
S Phase
Signal Transduction
Time Factors
Reg. No./Substance:
0/Cdkn1a protein, mouse; 0/Cyclin D; 0/Cyclin E; 0/Cyclin-Dependent Kinase Inhibitor Proteins; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Cyclins; 0/Retinoblastoma Protein; 147604-94-2/Cyclin-Dependent Kinase Inhibitor p27; EC Kinase 2; EC Kinase 4; EC Kinase 6; EC Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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