JBC

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J. Biol. Chem., Vol. 282, Issue 21, 99915, May 25, 2007
This Article
Right arrow Full Text (PDF)
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 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 Google Scholar
Google Scholar
Right arrow Search for Related Content
Related Collections
Right arrow Papers Of The Week
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?

A Scaffold for the D1 Dopamine Receptor{diamondsuit}

An important issue in understanding cell regulation is how the more than 600 G protein-coupled receptors found in mammalian genomes are organized in cells to generate specific responses to extracellular signals. One mechanism for this organization is via association with scaffolding proteins that can direct the receptors' interactions with other proteins, their signaling properties, and their intracellular trafficking. One of these scaffolding proteins is PSD-95. Located in the postsynaptic densities of central synapses, PSD-95 regulates N-methyl-D-aspartate receptor internalization, synaptic transmission, and plasticity and plays essential roles in learning.Go


Figure 1
D1 co-localizes with PSD-95.

In this Paper of the Week, Jingping Zhang and colleagues show that PSD-95 interacts with the D1 dopamine receptor to regulate its trafficking and function. Interestingly, this interaction is mediated by the carboxyl-terminal tail of D1 and the N terminus of PSD-95, a region of PSD-95 that has only recently been recognized as a participant in protein-protein interaction. Co-expression of PSD-95 with D1 inhibited D1-mediated cAMP accumulation by reducing D1 expression at the cell surface. In addition, genetically engineered mice lacking PSD-95 showed a heightened behavioral response to either a D1 agonist or the psychostimulant amphetamine. These studies characterize a potential site for coordinating glutamatergic and dopaminergic signaling and are likely to have a consequence for mechanisms involved in substance dependence and abuse.

FOOTNOTES

{diamondsuit} See referenced article, J. Biol. Chem. 2007, 282, 15778-15789 Back



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
Right arrow Full Text (PDF)
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 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 Google Scholar
Google Scholar
Right arrow Search for Related Content
Related Collections
Right arrow Papers Of The Week
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?


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2007 by the American Society for Biochemistry and Molecular Biology.