Distinct Patterns of Cleavage and Translocation of Cell Cycle Control Proteins in CD95-induced and p53-induced apoptosis.
10.3346/jkms.2003.18.4.467
- Author:
Weon Seo PARK
1
;
Kyeong Cheon JUNG
;
Doo Hyun CHUNG
;
Woo Dong NAM
;
Won Jin CHOI
;
Youngmee BAE
Author Information
1. Department of Pathology, Kangwon National University College of Medicine, Korea. ymbae@kangwon.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Etoposide;
Cell Cycle;
Nuclear Translocation;
Caspase;
DNA Damage;
poptosis
- MeSH:
Active Transport, Cell Nucleus;
Antigens, CD95/*metabolism;
*Apoptosis;
Cell Cycle;
Cell Nucleus/metabolism;
Coculture;
Dose-Response Relationship, Drug;
Down-Regulation;
Etoposide/pharmacology;
Flow Cytometry;
Human;
Immunoblotting;
Jurkat Cells;
Nucleic Acid Synthesis Inhibitors/pharmacology;
Protein Binding;
Protein Transport;
Protein p53/*metabolism;
Signal Transduction;
Up-Regulation
- From:Journal of Korean Medical Science
2003;18(4):467-472
- CountryRepublic of Korea
- Language:English
-
Abstract:
Apoptotic cell death induced by p53 occurs at a late G1 cell cycle checkpoint termed the restriction(R)point, and it has been proposed that p53-induced apoptosis causes upregulation of CD95. However, as cells with defective in CD95 signaling pathway are still sensitive to p53-induced apoptosis, CD95 cannot be the sole factor resulting in apoptosis. In addition, unlike p53-induced apoptosis, the relationship between CD95-mediated apoptosis and the cell cycle is not clearly understood. It would there-fore be worth investigating whether CD95-mediated cell death is pertinent with p53-induced apoptosis in view of cell cycle related molecules. In this report, biochemical analysis showed that etoposide-induced apoptosis caused the induction and the nuclear translocation of effector molecules involved in G1 cell cycle checkpoint. However, there was no such translocation in the case of CD95-mediated death. Thus, although both types of apoptosis involved caspase activation, the cell cycle related proteins responded differently. This argues against the idea that p53-induced apoptosis occurs through the induction of CD95/CD95L expression.
