3 results match your criteria: "Germany Center for Behavioral Brain Sciences (CBBS)[Affiliation]"

ZDHHC3 Tyrosine Phosphorylation Regulates Neural Cell Adhesion Molecule Palmitoylation.

Mol Cell Biol

September 2016

Department of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genoa, Italy Molecular Neuroplasticity Group, DZNE, Magdeburg, Germany Medical Faculty, Otto von Guericke University, Magdeburg, Germany Center for Behavioral Brain Sciences (CBBS), Magdeburg, Germany

The neural cell adhesion molecule (NCAM) mediates cell-cell and cell-matrix adhesion. It is broadly expressed in the nervous system and regulates neurite outgrowth, synaptogenesis, and synaptic plasticity. Previous in vitro studies revealed that palmitoylation of NCAM is required for fibroblast growth factor 2 (FGF2)-stimulated neurite outgrowth and identified the zinc finger DHHC (Asp-His-His-Cys)-containing proteins ZDHHC3 and ZDHHC7 as specific NCAM-palmitoylating enzymes.

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Synapsin is required to "boost" memory strength for highly salient events.

Learn Mem

January 2016

Leibniz Institut für Neurobiologie (LIN), Abteilung Genetik von Lernen und Gedächtnis, 39118 Magdeburg, Germany Center for Behavioral Brain Sciences (CBBS), Magdeburg, Germany Otto von Guericke Universität Magdeburg, Institut für Biologie, 39106 Magdeburg, Germany

Synapsin is an evolutionarily conserved presynaptic phosphoprotein. It is encoded by only one gene in the Drosophila genome and is expressed throughout the nervous system. It regulates the balance between reserve and releasable vesicles, is required to maintain transmission upon heavy demand, and is essential for proper memory function at the behavioral level.

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Hyaluronan-based extracellular matrix under conditions of homeostatic plasticity.

Philos Trans R Soc Lond B Biol Sci

October 2014

Department for Neurochemistry and Molecular Biology, Leibniz Institute for Neurobiology Magdeburg, Magdeburg, Germany Center for Behavioral Brain Sciences (CBBS) Magdeburg, Magdeburg, Germany

Neuronal networks are balanced by mechanisms of homeostatic plasticity, which adjusts synaptic strength via molecular and morphological changes in the pre- and post-synapse. Here, we wondered whether the hyaluronic acid-based extracellular matrix (ECM) of the brain is involved in mechanisms of homeostatic plasticity. We hypothesized that the ECM, being rich in chondroitin sulfate proteoglycans such as brevican, which are suggested to stabilize synapses by their inhibitory effect on structural plasticity, must be remodelled to allow for structural and molecular changes during conditions of homeostatic plasticity.

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