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Overexpression of Par-4 Enhances Thapsigargin-Induced Apoptosis Via Down-Regulation of XIAP and Inactivation of Akt in Human Renal Cancer Cells

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Author(s)
Tae-Jin LeeJung-Tae LeeSang Hyun KimYung Hyun ChoiKyoung Seob SongJong-Wook ParkTaeg Kyu Kwon
Keimyung Author(s)
Park, Jong WookKwon, Taeg Kyu
Department
Dept. of Immunology (면역학)
Institute for Medical Science (의과학연구소)
Journal Title
Journal of Cellular Biochemistry
Issued Date
2008
Volume
103
Issue
2
Keyword
Par-4XIAPpAktER-stressthapsigargin (TG)
Abstract
The prostate-apoptosis-response-gene-4 (Par-4) protein has been shown to function as an effector of cell death in response to various apoptotic stimuli that trigger mitochondria and membrane receptor-mediated cell death pathways. We found that overexpressing Par-4 by stable transfection sensitizes Caki cells to induction of apoptosis by TRAIL and drugs that induce endoplasmic reticulum (ER) stress [thapsigargin (TG), tunicamycin (TU) and etoposide]. Ectopic expression of Par-4 is associated with decreased levels of XIAP protein in TG-treated cells, caused in part by XIAP protein instability and caspase activation. Levels of phospho-Akt are decreased in Caki/Par-4 cells to a significantly greater extent than in Caki/Vector cells by treatment with TG, and this is in turn associated with decreased levels of phospho-PDK1, the kinase upstream of Akt. In conclusion, we provide evidence that ectopic expression of Par-4 sensitizes Caki cells to TG and that XIAP protein instability and inactivation of Akt are important in cellular pathways affected by Par-4.
Keimyung Author(s)(Kor)
박종욱
권택규
Publisher
School of Medicine
Citation
Tae-Jin Lee et al. (2008). Overexpression of Par-4 Enhances Thapsigargin-Induced Apoptosis Via Down-Regulation of XIAP and Inactivation of Akt in Human Renal Cancer Cells. Journal of Cellular Biochemistry, 103(2), 358–368. doi: 10.1002/jcb.21642
Type
Article
ISSN
0730-2312
Source
http://lps3.onlinelibrary.wiley.com.proxy.dsmc.or.kr/doi/abs/10.1002/jcb.21642
DOI
10.1002/jcb.21642
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/33970
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
3. Research Institutues (연구소) > Institute for Medical Science (의과학연구소)
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