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The Ras1–Mitogen-Activated Protein Kinase Signal Transduction Pathway Regulates Synaptic Plasticity through Fasciclin II-Mediated Cell Adhesion

The Ras1–Mitogen-Activated Protein Kinase Signal Transduction Pathway Regulates Synaptic... The Journal of Neuroscience, April 1, 2002, 22(7):2496–2504 The Ras1–Mitogen-Activated Protein Kinase Signal Transduction Pathway Regulates Synaptic Plasticity through Fasciclin II-Mediated Cell Adhesion Young-Ho Koh, Catalina Ruiz-Canada, Michael Gorczyca, and Vivian Budnik Department of Biology, Neuroscience and Behavior Program, University of Massachusetts, Amherst, Massachusetts Ras proteins are small GTPases with well known functions in junction, and modification of their activity levels results in an cell proliferation and differentiation. In these processes, they altered number of synaptic boutons. Gain- or loss-of-function play key roles as molecular switches that can trigger distinct mutations in Ras1 and MAPK reveal that regulation of synapse signal transduction pathways, such as the mitogen-activated structure by this signal transduction pathway is dependent on protein kinase (MAPK) pathway, the phosphoinositide-3 kinase fasciclin II localization at synaptic boutons. These results pro- pathway, and the Ral–guanine nucleotide dissociation stimula- vide evidence for a Ras-dependent signaling cascade that tor pathway. Several studies have implicated Ras proteins in regulates fasciclin II-mediated cell adhesion at synaptic termi- the development and function of synapses, but the molecular nals during synapse growth. mechanisms for this regulation are poorly understood. Here, we demonstrate that the Ras–MAPK pathway is involved in syn- Key words: mitogen-activated protein http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neuroscience Unpaywall

The Ras1–Mitogen-Activated Protein Kinase Signal Transduction Pathway Regulates Synaptic Plasticity through Fasciclin II-Mediated Cell Adhesion

Koh, Young-Ho; Ruiz-Canada, Catalina; Gorczyca, Michael; Budnik, Vivian
Journal of Neuroscience – Apr 1, 2002
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Publisher
Unpaywall
ISSN
0270-6474
DOI
10.1523/jneurosci.22-07-02496.2002
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Abstract

The Journal of Neuroscience, April 1, 2002, 22(7):2496–2504 The Ras1–Mitogen-Activated Protein Kinase Signal Transduction Pathway Regulates Synaptic Plasticity through Fasciclin II-Mediated Cell Adhesion Young-Ho Koh, Catalina Ruiz-Canada, Michael Gorczyca, and Vivian Budnik Department of Biology, Neuroscience and Behavior Program, University of Massachusetts, Amherst, Massachusetts Ras proteins are small GTPases with well known functions in junction, and modification of their activity levels results in an cell proliferation and differentiation. In these processes, they altered number of synaptic boutons. Gain- or loss-of-function play key roles as molecular switches that can trigger distinct mutations in Ras1 and MAPK reveal that regulation of synapse signal transduction pathways, such as the mitogen-activated structure by this signal transduction pathway is dependent on protein kinase (MAPK) pathway, the phosphoinositide-3 kinase fasciclin II localization at synaptic boutons. These results pro- pathway, and the Ral–guanine nucleotide dissociation stimula- vide evidence for a Ras-dependent signaling cascade that tor pathway. Several studies have implicated Ras proteins in regulates fasciclin II-mediated cell adhesion at synaptic termi- the development and function of synapses, but the molecular nals during synapse growth. mechanisms for this regulation are poorly understood. Here, we demonstrate that the Ras–MAPK pathway is involved in syn- Key words: mitogen-activated protein

Journal

Journal of Neuroscience – Unpaywall

Published: Apr 1, 2002

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