Advertisement
J. Lipid Res.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


A more recent version of this article appeared on December 1, 2005

Papers In Press, published online ahead of print October 1, 2005
J. Lipid Res., doi:10.1194/jlr.M500252-JLR200
This Article
Right arrow Full Text (Accepted Manuscript)
Right arrow All Versions of this Article:
M500252-JLR200v1
46/12/2580    most recent
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 arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chen, X.
Right arrow Articles by Yang, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chen, X.
Right arrow Articles by Yang, F.
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?

Submitted on June 16, 2005
Revised on September 19, 2005
Accepted on September 30, 2005

Inhibitory effect of ganglioside GD1b on K+ current in hippocampal neurons and its involvement in cell apoptosis suppression

Xuesong Chen, Shaopeng Chi, Mingna Liu, Wei Yang, Taotao Wei, Zhi Qi, and Fuyu Yang

State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, Beijing 100101

Corresponding Author: qizhi{at}sun5.ibp.ac.cn

Gangliosides are endogenous membrane components enriched in neuronal cells. They have been shown to play regulatory roles in many cellular processes. Here, we show for the first time that ganglioside GD1b plays an anti-apoptotic role in cultured hippocampal neurons. GD1b inhibited the outward delayed rectifier IK current but not the transient outward IA current in a dose-dependent manner with IC50 value of 15.2 mu M. Such effect appears to be somehow specific, since GD1b, but not GM1, GM2, GM3, GD1a, GD3 or GT1b, was effective on inhibiting IK current. Intracellular application of STS (0.1mu M) resulted in rapid activation of IK, which was partially reversed upon addition of K+ channel blocker tetraethylammonium (TEA, 5 mM) and GD1b (10 mu M). Furthermore, GD1b (10 mu M) attenuated staurosporine-induced neuronal apoptosis by nearly the same as that of 5 mM TEA. In addition, GD1b suppressed the apoptosis-associated capase 3 activation that was activated by STS. Collectively, these findings implicate that GD1b plays an anti-apoptotic role in cultured hippocampal neurons through its inhibitory effect on the outward IK current and the caspase activity.


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?





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 All ASBMB Journals   Journal of Biological Chemistry 
 Molecular and Cellular Proteomics   ASBMB Today 
Copyright © 2005 by the American Society for Biochemistry and Molecular Biology.
Advertisement
spacer
Advertisement
Advertisement