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J. Biol. Chem., Vol. 280, Issue 37, 32419-32425, September 16, 2005

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Interactions with PDZ Domain Proteins PIST/GOPC and PDZK1 Regulate Intracellular Sorting of the Somatostatin Receptor Subtype 5^*

Wolf Wente1, Thomas Stroh, Alain Beaudet, Dietmar Richter2, and Hans-Jürgen Kreienkamp3

From the Institut für Zellbiochemie und klinische Neurobiologie and Institut für Humangenetik, Universitätskrankenhaus Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany and the Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada H3A 2B4

By yeast two-hybrid screening we have identified interaction partners for the intracellular C-terminal tail of the human and rodent somatostatin receptor subtype 5 (SSTR5). Interactions with the PDZ domain-containing proteins PIST and PDZK1 are mediated by the PDZ ligand motif at the C terminus of the receptor; in case of the human and mouse (but not the rat) receptors, a slight sequence variation of this motif also allows for binding of the peroxisomal receptor PEX5. PIST is Golgi-associated and retains SSTR5 in the Golgi apparatus when coexpressed with the receptor; PDZK1 on the other hand associates with the SSTR5 at the plasma membrane. Endogenous SSTR5 in the neuroendocrine AtT-20 tumor cell line is colocalized with PIST in the Golgi apparatus. On a functional level, removal of the PDZ ligand motif of the receptor does not interfere with agonist-dependent internalization of the receptor or its targeting to a Golgi-associated compartment; however, recycling of the receptor to the plasma membrane after washout of the agonist is inhibited, suggesting that the PDZ-mediated interaction of SSTR5 is required for postendocytic sorting.

Received for publication, July 1, 2005

^* This work was supported by Deutsche Forschungsgemeinschaft (SFB545/B7 to D. R. and H.-J. K.), the Canadian Institutes of Health Research (MOP-7366 to A. B.), and the European commission (QLG3-CT-1999-00908 to D. R.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Submitted as part of a Ph.D. thesis at the University of Hamburg, Germany.

² To whom correspondence may be addressed. E-mail: Richter{at}uke.uni_hamburg.de. ³ To whom correspondence may be addressed: Institut für Humangenetik, Universitätskrankenhaus Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. Tel.: 49-40-42803-4395; Fax: 49-40-42803-5098; E-mail: Kreienkamp{at}uke.uni-hamburg.de.

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