Neuronal Ca2+ sensor protein VILIP-1 affects cGMP signalling of guanylyl cyclase B by regulating clathrin-dependent receptor recycling in hippocampal neurons
Author:
Brackmann Marian1, Schuchmann Sebastian2, Anand Rene3, Braunewell Karl-Heinz1
Affiliation:
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
Abstract
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.
Publisher
The Company of Biologists
Reference50 articles.
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