Rapid Signaling Of Estrogen To Neuronal Dendrite Spine Formation - Softcover
Estrogens are important regulators of neuronal cell morphology and this is thought to be critical for gender-specific differences in brain function and dysfunction. Dendritic spine formation is dependent on actin remodeling by WAVE1 protein, which controls actin polymerization through the Arp-2/3 complex. We show that 17-estradiol (E2) administration leads to phosphorylation and redistribution of WAVE1 at sites of dendritic spine formation. WAVE1 phosphorylation is found to be triggered by a Gαi/Gβ protein-dependent, rapid extranuclear signaling of ERα to Src/Rac1/Cdk5 that directly phosphorylates WAVE1. After WAVE1 phosphorylation, the Arp-2/3 complex concentrates at sites of spine formation, where it triggers the local reorganization of actin fibers. In parallel, E2 recruits a Gα13-dependent pathway to RhoA and ROCK-2, leading to activation of actin remodeling via moesin. Silencing of WAVE1 or of moesin abrogates the increase in dendritic spines induced by E2. In conclusion, our findings indicate that the control of actin polymerization and branching via moesin or WAVE1 is a key function of ERα in neurons, which may be particularly relevant for the regulation of dendritic spines.
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Born in Argentina in 1977, he obtained his degree in Molecular Biology from National University of San Luis in 2004. In 2006 he was incorporated at MCGEL laboratory where he began to study neuronal and breast cancer cell movement, and in 2010 he received the Ph.D. from Pisa University. In 2011 he was incorporated at IMBECU-CONICET Mendoza.
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- PublisherLAP LAMBERT Academic Publishing
- Publication date2012
- ISBN 10 3847317466
- ISBN 13 9783847317463
- BindingPaperback
- Number of pages92
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Rapid Signaling Of Estrogen To Neuronal Dendrite Spine Formation
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Book Description Taschenbuch. Condition: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -Estrogens are important regulators of neuronal cell morphology and this is thought to be critical for gender-specific differences in brain function and dysfunction. Dendritic spine formation is dependent on actin remodeling by WAVE1 protein, which controls actin polymerization through the Arp-2/3 complex. We show that 17-estradiol (E2) administration leads to phosphorylation and redistribution of WAVE1 at sites of dendritic spine formation. WAVE1 phosphorylation is found to be triggered by a G i/G protein-dependent, rapid extranuclear signaling of ER to Src/Rac1/Cdk5 that directly phosphorylates WAVE1. After WAVE1 phosphorylation, the Arp-2/3 complex concentrates at sites of spine formation, where it triggers the local reorganization of actin fibers. In parallel, E2 recruits a G 13-dependent pathway to RhoA and ROCK-2, leading to activation of actin remodeling via moesin. Silencing of WAVE1 or of moesin abrogates the increase in dendritic spines induced by E2. In conclusion, our findings indicate that the control of actin polymerization and branching via moesin or WAVE1 is a key function of ER in neurons, which may be particularly relevant for the regulation of dendritic spines. 92 pp. Englisch. Seller Inventory # 9783847317463
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Rapid Signaling Of Estrogen To Neuronal Dendrite Spine Formation
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Book Description Taschenbuch. Condition: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - Estrogens are important regulators of neuronal cell morphology and this is thought to be critical for gender-specific differences in brain function and dysfunction. Dendritic spine formation is dependent on actin remodeling by WAVE1 protein, which controls actin polymerization through the Arp-2/3 complex. We show that 17-estradiol (E2) administration leads to phosphorylation and redistribution of WAVE1 at sites of dendritic spine formation. WAVE1 phosphorylation is found to be triggered by a G i/G protein-dependent, rapid extranuclear signaling of ER to Src/Rac1/Cdk5 that directly phosphorylates WAVE1. After WAVE1 phosphorylation, the Arp-2/3 complex concentrates at sites of spine formation, where it triggers the local reorganization of actin fibers. In parallel, E2 recruits a G 13-dependent pathway to RhoA and ROCK-2, leading to activation of actin remodeling via moesin. Silencing of WAVE1 or of moesin abrogates the increase in dendritic spines induced by E2. In conclusion, our findings indicate that the control of actin polymerization and branching via moesin or WAVE1 is a key function of ER in neurons, which may be particularly relevant for the regulation of dendritic spines. Seller Inventory # 9783847317463
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Book Description Condition: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Autor/Autorin: Angel Matias SanchezBorn in Argentina in 1977, he obtained his degree in Molecular Biology from National University of San Luis in 2004. In 2006 he was incorporated at MCGEL laboratory where he began to study neuronal and breast canc. Seller Inventory # 5509640
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