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La kinase neuronale PAK3 :
Etude des trois mutations responsables de retard mental non syndromique et mise en évidence de deux nouveaux variants d'épissage

Abstract : The p21-activated kinase 3 (PAK3) codes for a serine threonine protein kinase implicated in non syndromique mental retardation. PAK kinases are activated by the GTPases Cdc42 and Rac1 and regulate neuronal plasticity through actin cytoskeleton. In order to understand the specific role of PAK3 in cognitive functions, we studied the mutations responsible for mental retardation and characterized new splice variants. We show that: 1) PAK3 is selectively activated by Cdc42; 2) two mutations totally abolish the kinase activity and profoundly alter dendritic spine morphology; 3) a third mutation decreases the binding of PAK3 to the GTPase Cdc42 and drastically reduces spine density. These results suggest that Cdc42/PAK3 is a key module in dendritic spine formation and synaptic plasticity. We also identified two new constitutively active PAK3 splice variants and propose a new regulation model of their kinase activity, based on the formation of heterodimers.
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https://tel.archives-ouvertes.fr/tel-00199812
Contributor : Patricia Kreis <>
Submitted on : Wednesday, December 19, 2007 - 4:10:53 PM
Last modification on : Thursday, January 11, 2018 - 6:19:38 AM
Long-term archiving on: : Monday, April 12, 2010 - 8:33:48 AM

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  • HAL Id : tel-00199812, version 1

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Patricia Kreis. La kinase neuronale PAK3 :
Etude des trois mutations responsables de retard mental non syndromique et mise en évidence de deux nouveaux variants d'épissage. Neurosciences [q-bio.NC]. Université Paris Sud - Paris XI, 2007. Français. ⟨tel-00199812⟩

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