Nerve Growth Factor Attenuates Endoplasmic Reticulum Stress-Mediated Apoptosis <i>via</i> Suppression of Caspase-12 Activity
-
- Shimoke Koji
- Laboratory of Neurobiology, Faculty of Engineering and High Technology Research Center (HRC), Kansai University
-
- Amano Hisayuki
- Laboratory of Neurobiology, Faculty of Engineering and High Technology Research Center (HRC), Kansai University
-
- Kishi Soichiro
- Laboratory of Neurobiology, Faculty of Engineering and High Technology Research Center (HRC), Kansai University
-
- Uchida Hitoshi
- Laboratory of Neurobiology, Faculty of Engineering and High Technology Research Center (HRC), Kansai University
-
- Kudo Motoshige
- Second Department of Pathology, Tokyo Medical University
-
- Ikeuchi Toshihiko
- Laboratory of Neurobiology, Faculty of Engineering and High Technology Research Center (HRC), Kansai University
Bibliographic Information
- Other Title
-
- Nerve Growth Factor Attenuates Endoplasmic Reticulum Stress-Mediated Apoptosis via Suppression of Caspase-12 Activity
Search this article
Abstract
Following endoplasmic reticulum (ER) stress, which occurs via inhibition of the glyc-osylation of newly synthesized proteins, caspase family proteins are activated to promote ER stress-mediated apoptosis. Here we report that nerve growth factor (NGF) suppressed the ER stress-mediated apoptosis in tunicamycin-treated PC12 cells through an extensive decrease of the caspase-3/-9/-12 activity. Detailed analysis of the mechanism underlying the NGF-mediated cell survival revealed that the activities of all seriate caspases were reduced through the phosphatidylinositol 3-kinase (PI3-K) signaling pathway induced by NGF. Moreover, we found that the activity of c-Jun N-terminal kinase (JNK) was not essential for the tunicamycin-induced apoptosis of PC 12 cells. These results demonstrate that the inactivation of caspase-12 via the NGFmediated PI3-K signaling pathway leads to inactivation of the caspase cascade including caspase-3 and -9.
Journal
-
- The Journal of Biochemistry
-
The Journal of Biochemistry 135 (3), 439-446, 2004
The Japanese Biochemical Society
- Tweet
Details 詳細情報について
-
- CRID
- 1390001204965534592
-
- NII Article ID
- 130003534681
- 10016199170
-
- NII Book ID
- AA00694073
-
- COI
- 1:CAS:528:DC%2BD2cXjvFKisbo%3D
-
- ISSN
- 17562651
- 0021924X
-
- NDL BIB ID
- 6904076
-
- PubMed
- 15113843
-
- Text Lang
- en
-
- Data Source
-
- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
-
- Abstract License Flag
- Disallowed