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A link between cell cycle and cell death: Bax and Bcl‐2 modulate Cdk2 activation during thymocyte apoptosis
Author(s) -
GilGómez Gabriel,
Berns Anton,
Brady Hugh J.M.
Publication year - 1998
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/17.24.7209
Subject(s) - biology , apoptosis , cyclin dependent kinase 2 , programmed cell death , microbiology and biotechnology , cell cycle , thymocyte , link (geometry) , cancer research , genetics , t cell , immune system , computer network , computer science
Resting thymocytes undergoing apoptosis in response to specific stimuli degrade the cdk inhibitor p27 Kip1 and upregulate Cdk2 kinase activity. Inhibition of Cdk2 kinase activity efficiently blocks cell death via certain apoptosis pathways whereas overexpression of Cdk2 accelerates such cell death, suggesting its involvement in the signal transduction pathways activated by certain apoptotic stimuli. We found that Cdk2 activation during thymocyte apoptosis can be regulated by p53, Bax and Bcl‐2. The highly elevated Cdk2 kinase activity in the apoptosing thymocytes is not associated with its canonical cyclins, cyclin E and cyclin A, and requires de novo synthesis of proteins for activation to take place. We therefore propose Cdk2 activation to be a crucial event in distinct pathways of apoptosis and the point at which the cell cycle and cell death pathways interact.