Cited 0 times in

TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt

Title
TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt
Authors
BO K. SUN;JOO-HANG KIM;JAE J. SONG;YONG J. LEE;SEEUN OH;SO Y. KIM;HOAN N. NGUYEN
Issue Date
2011
Journal Title
International Journal of Oncology
ISSN
1019-6439
Citation
International Journal of Oncology, Vol.38(1) : 249~256, 2011
Abstract
We previously observed that TRAIL induces acquired TRAIL resistance coinciding with increased Akt phosphorylation brought about by the Src-PI3K-Akt signaling pathways and mediated by c-Cbl. c-Cbl, a ubiquitously expressed cytoplasmic adaptor protein, is simultaneously involved in the rapid degradation of TRAIL receptors and Akt phosphorylation during TRAIL treatment. Here, we show that Akt phosphorylation is not exclusively responsible for acquired TRAIL resistance. Akt catalytic activation is known to increase during metabolic oxidative stress, but we show that TRAIL also dramatically induces the catalytic activation of Akt in TRAIL-sensitive cells, but not in TRAIL-resistant cells. This suggests that Akt catalytic activation during TRAIL-induced apoptosis is likely to play a compensatory role in the maintenance of cell homeostasis. In addition, activated p38 and phosphorylated HSP27 were found to act as downstream effector molecules of p38 during TRAIL treatment and were shown to be responsible for increased Akt catalytic and invasive activities
URI

http://ir.ymlib.yonsei.ac.kr/handle/22282913/92569
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Medical Research Center
1. 연구논문 > 5. Research Institutes > Institute for Cancer Research
1. 연구논문 > 1. College of Medicine > Dept. of Internal Medicine
1. 연구논문 > 1. College of Medicine > Yonsei Biomedical Research Center
Yonsei Authors
사서에게 알리기
  feedback
Files in This Item:
T201100143.pdfDownload
Export
RIS (EndNote)
XLS (Excel)
XML

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse