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ID 24972
file
creator
Hyoda, Kanae
Horie, Naohiro
Okuma, Yasunobu
Nomura, Yasuyuki
subject
endoplasmic reticulum stress
P13K-Akt pathway
LY294002
Wortmannin
PD98059
CHOP
NDC
Medical sciences
abstract
Stress signals that impair the function of the endoplasmic reticulum (ER) can lead to an accumulation of unfolded proteins in the ER causing cell death. Recent studies have indicated that ER stress contributes to several diseases such as neurodegenerative disorders or diabetes. In the present study, we found that Akt down-regulation is important for inducing CHOP expression, an ER stress-induced transcription factor. Treatment with tunicamycin or thapsigargin, ER stress inducers, caused dephosphorylation of Akt from 12 to 24 h and induced cell death. Interestingly, treatment with a PI3K inhibitor alone induced CHOP expression and caused cell death. However, a MEK 1 inhibitor induced neither CHOP expression nor cell death. These results indicate that the inactivation of Akt by ER stress induces CHOP expression and causes cell death. Therefore, Akt plays an important role in ER stressed condition and may have important implications for understanding ER stress-related diseases.
journal title
Biochemical and Biophysical Research Communications
volume
Volume 340
issue
Issue 1
start page
286
end page
290
date of issued
2006-02-03
publisher
Elsevier Inc.
issn
0006-291X
ncid
publisher doi
language
eng
nii type
Journal Article
HU type
Journal Articles
DCMI type
text
format
application/pdf
text version
author
rights
Copyright (c) 2006 Elsevier Inc.
relation is version of URL
http://dx.doi.org/10.1016/j.bbrc.2005.12.007
department
Graduate School of Biomedical Science