ID 110735
Author
Ohtani, Naoko Division of Protein Information, Institute for Genome Research, The University of Tokushima
Yamakoshi, Kimi Division of Protein Information, Institute for Genome Research, The University of Tokushima
Takahashi, Akiko Division of Protein Information, Institute for Genome Research, The University of Tokushima Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Hara, Eiji Division of Protein Information, Institute for Genome Research, The University of Tokushima
Keywords
cellular senescence
cell cycle control
tumor suppression
p16INK4a
Content Type
Journal Article
Description
The p16INK4a tumor suppressor protein functions as an inhibitor ofCDK4andCDK6, the D-type cyclin-dependent kinases that initiate the phosphorylation of the retinoblastoma tumor suppressor protein, RB. Thus, p16INK4a has the capacity to arrest cells in the G1-phase of the cell cycle and its probable physiological role is in the implementation of irreversible growth arrest termed cellular senescence. Cellular senescence is a state of permanent growth arrest that can be induced by a variety of stresses such as DNA-damage and aberrant mitogenic signaling in human primary cells. In contrast to normal cells, the function of the p16INK4a gene or its downstream mediators is frequently deregulated in many types of human cancers, illustrating the importance of cellular senescence in tumor suppression. Here we discuss the molecular mechanisms that direct cellular senescence and reveal its potential for tumor suppression.
Journal Title
The journal of medical investigation : JMI
ISSN
13431420
NCID
AA11166929
Volume
51
Issue
3-4
Start Page
146
End Page
153
Sort Key
146
Published Date
2004-08
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher
departments
Center of University Education