JBC Advanced Glycation Endproducts

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

A more recent version of this article appeared on December 3, 2004
This Article
Right arrow Full Text (Accepted Manuscript)
Right arrow All Versions of this Article:
279/49/51182    most recent
M407225200v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yasuoka, C.
Right arrow Articles by Kohno, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yasuoka, C.
Right arrow Articles by Kohno, S.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Papers In Press, published online ahead of print September 16, 2004
J. Biol. Chem, 10.1074/jbc.M407225200
Submitted on June 28, 2004
Revised on September 3, 2004
Accepted on September 15, 2004

Antiapoptotic activity of Akt is down-regulated by Ca2+ in myocardiac H9c2 cells Evidence of Ca2+-dependent regulation of protein phosphatase 2Ac

Chie Yasuoka, Yoshito Ihara, Satoshi Ikeda, Yoshiyuki Miyahara, Takahito Kondo, and Shigeru Kohno

Department of Biochemistry and Molecular Biology in Disease, Nagasaki University, Nagasaki, Nagasaki 852-8523

Corresponding Author: y-ihara{at}net.nagasaki-u.ac.jp

Cell survival signaling of the Akt/protein kinase B pathway was influenced by a change in the cytoplasmic free calcium concentration ([Ca2+]i) for over 2 hours via the regulation of a Ser/Thr phosphatase, protein phosphatase 2Ac (PP2Ac), in rat myocardiac H9c2 cells. Akt was down-regulated when [Ca2+]i was elevated by thapsigargin, an inhibitor of the endoplasmic reticulum Ca2+-ATPase, but was up-regulated when it was suppressed by 1,2-bis (o-aminophenoxy) ethane-N,N,N,N-tetraacetic acid tetra (acetoxymethyl) ester (BAPTA-AM), a cell permeable Ca2+ chelator. The inactivation of Akt was well correlated with the susceptibility to oxidant-induced apoptosis in H9c2 cells. To investigate the mechanism of the Ca2+-dependent regulation of Akt via the regulation of PP2A, we examined the transcriptional regulation of PP2Aca in H9c2 cells with Ca2+ modulators. Transcription of the PP2Aca gene was increased by thapsigargin but decreased by BAPTA-AM. The promoter activity was examined and the cAMP response element (CRE) was found responsible for the Ca2+-dependent regulation of PP2Aca. Furthermore, phosphorylation of CRE-binding protein increased with thapsigargin but decreased with BAPTA-AM. A long-term change of [Ca2+]i regulates PP2Aca gene transcription via CRE, resulting in a change in the activation status of Akt leading to an altered susceptibility to apoptosis.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
B. S. Marasa, L. Xiao, J. N. Rao, T. Zou, L. Liu, J. Wang, E. Bellavance, D. J. Turner, and J.-Y. Wang
Induced TRPC1 expression increases protein phosphatase 2A sensitizing intestinal epithelial cells to apoptosis through inhibition of NF-{kappa}B activation
Am J Physiol Cell Physiol, May 1, 2008; 294(5): C1277 - C1287.
[Abstract] [Full Text] [PDF]

Home page
 GlycobiologyHome page
E. Muroi, S. Manabe, M. Ikezaki, Y. Urata, S. Sato, T. Kondo, Y. Ito, and Y. Ihara
C-Mannosylated peptides derived from the thrombospondin type 1 repeat enhance lipopolysaccharide-induced signaling in macrophage-like RAW264.7 cells
Glycobiology, September 1, 2007; 17(9): 1015 - 1028.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
T.-Y. Chin, H.-C. Lin, J.-P. Kuo, and S.-H. Chueh
Dual effect of thapsigargin on cell death in porcine aortic smooth muscle cells
Am J Physiol Cell Physiol, January 1, 2007; 292(1): C383 - C395.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
Y. Hayashida, Y. Urata, E. Muroi, T. Kono, Y. Miyata, K. Nomata, H. Kanetake, T. Kondo, and Y. Ihara
Calreticulin Represses E-cadherin Gene Expression in Madin-Darby Canine Kidney Cells via Slug
J. Biol. Chem., October 27, 2006; 281(43): 32469 - 32484.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
T. Okunaga, Y. Urata, S. Goto, T. Matsuo, S. Mizota, K. Tsutsumi, I. Nagata, T. Kondo, and Y. Ihara
Calreticulin, a Molecular Chaperone in the Endoplasmic Reticulum, Modulates Radiosensitivity of Human Glioblastoma U251MG Cells.
Cancer Res., September 1, 2006; 66(17): 8662 - 8671.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
Y. Urata, Y. Ihara, H. Murata, S. Goto, T. Koji, J. Yodoi, S. Inoue, and T. Kondo
17beta-Estradiol Protects against Oxidative Stress-induced Cell Death through the Glutathione/Glutaredoxin-dependent Redox Regulation of Akt in Myocardiac H9c2 Cells
J. Biol. Chem., May 12, 2006; 281(19): 13092 - 13102.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
Y. Ihara, Y. Urata, S. Goto, and T. Kondo
Role of calreticulin in the sensitivity of myocardiac H9c2 cells to oxidative stress caused by hydrogen peroxide
Am J Physiol Cell Physiol, January 1, 2006; 290(1): C208 - C221.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2004 by the American Society for Biochemistry and Molecular Biology.