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First published online May 28, 2005
doi: 10.1242/10.1242/jcs.02376

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Neuronal Ca²⁺ sensor protein VILIP-1 affects cGMP signalling of guanylyl cyclase B by regulating clathrin-dependent receptor recycling in hippocampal neurons

¹ Signal Transduction Research Group, Charité, University Medicine, 10117 Berlin, Germany
² Neuroscience Research Center, Charité, University Medicine, 10117 Berlin, Germany
³ Neuroscience Center of Excellence and Department of Neurology, Louisiana State University Health Sciences Center, New Orleans, LA, 70112, USA

^* Author for correspondence (e-mail: karl-heinz.braunewell{at}charite.de)

Accepted 14 March 2005

The family of neuronal Ca²⁺ sensor (NCS) proteins is known to influence a variety of physiological and pathological processes by affecting signalling of different receptors and ion channels. Recently, it has been shown that the NCS protein VILIP-1 influences the activity of the receptor guanylyl cyclase GC-B. In transfected cell lines, VILIP-1 performs a Ca²⁺-dependent membrane association, the reversible Ca²⁺-myristoyl switch of VILIP-1, which leads to an increase in natriuretic peptide-stimulated cGMP levels. In this study, we have investigated the effect of VILIP-1 on cGMP signalling in C6 cells and in primary hippocampal neurons, where VILIP-1 and GC-B are co-expressed in many but not all neurons and partially co-localize in the soma and in dendrites. Our data indicate that VILIP-1 modulates GC-B activity by influencing clathrin-dependent receptor recycling. These data support a general physiological role for VILIP-1 in membrane trafficking in the intact hippocampus, where the NCS protein may affect processes, such as neuronal differentiation and synaptic plasticity e.g. by influencing cGMP-signalling.

Key words: Ca²⁺-binding protein, Guanylyl cyclase B, Hippocampus, Myristoylation, Receptor desensitization, Receptor recycling

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