RB-resistant Abl kinase induces delayed cell cycle progression and increases susceptibility to apoptosis upon cellular stresses through interaction with p53

Authors
Jae-We ChoJunah ChungWon-Ki BaekSeong-Il SuhTaeg Kyu KwonJong-Wook ParkMin-Ho Suh
Department
Dept. of Dermatology (피부과학); Dept. of Immunology (면역학); Dept. of Microbiology (미생물학)
Issue Date
2003
Citation
International Journal of Oncology, Vol.22(6) : 1193-1199, 2003
ISSN
1019-6439
Abstract
c-Abl, a non-receptor tyrosine kinase, is found in both nucleus and cytoplasm of proliferating fibroblasts. RB negatively regulates the kinase activity of c-Abl. Overexpression of kinase active c-Abl can overcome RB-induced growth arrest in Saos-2 cells. However, we previously reported that disruption of the RB matchmaker function leads to delayed cell cycle progression in the presence of p53. In this study, we investigated whether overexpression of mutant c-Abl (AS2, RB-resistant Abl kinase) not only lead to delayed cell cycle progression but also make cells susceptible to apoptosis under coexpression with a fragment of RB C pocket in human skin fibroblast. AS2 expressing cells showed delayed cell growth rate in normal growth condition. After genotoxic stress such as etoposide treatment, AS2 expressing cells readily progressed into apoptosis through p53 and caspase-3 activations. Our results suggest that expression of AS2 not only induces delayed cell cycle progression but also results in increased sensitivity to apoptosis in the presence of p53.
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35932
Appears in Collections:
1. Journal Papers (연구논문) > 1. School of Medicine (의과대학) > Dept. of Dermatology (피부과학)
1. Journal Papers (연구논문) > 1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
1. Journal Papers (연구논문) > 1. School of Medicine (의과대학) > Dept. of Microbiology (미생물학)
Keimyung Author(s)
조재위; 권택규; 박종욱; 백원기; 서민호; 서성일
Full Text
https://www.spandidos-publications.com/ijo/22/6/1193
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