|
|
|
|
|
|
|
||
J. Exp. Med.,
Volume 189, Number 6, March 15, 1999 957-968
By
From The Amgen Institute, the Ontario Cancer Institute, and the Department of Medical Biophysics
and the Department of Immunology, University of Toronto, Toronto, Ontario, Canada M5G 2C1
Aberrant activation of cell cycle molecules has been postulated to play a role in apoptosis ("catastrophic cell cycle"). Here we show that in noncycling developing thymocytes, the cyclin- dependent kinase Cdk2 is activated in response to all specific and nonspecific apoptotic stimuli
tested, including peptide-specific thymocyte apoptosis. Cdk2 was found to function upstream
of the tumor suppressor p53, transactivation of the death promoter Bax, alterations of mitochondrial permeability, Bcl-2, caspase activation, and caspase-dependent proteolytic cleavage
of the retinoblastoma protein. Inhibition of Cdk2 completely protected thymocytes from apoptosis, mitochondrial changes, and caspase activation. These data provide the first evidence that
Cdk2 activity is crucial for the induction of thymocyte apoptosis.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
| TABLE OF CONTENTS |
|
