2015
DOI: 10.1002/brb3.359
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Neuritic complexity of hippocampal neurons depends on WIP‐mediated mTORC1 and Abl family kinases activities

Abstract: IntroductionNeuronal morphogenesis is governed mainly by two interconnected processes, cytoskeletal reorganization, and signal transduction. The actin‐binding molecule WIP (Wiskott‐Aldrich syndrome protein [WASP]‐interacting protein) was identified as a negative regulator of neuritogenesis. Although WIP controls activity of the actin‐nucleation‐promoting factor neural WASP (N‐WASP) during neuritic differentiation, its implication in signal transduction remains unknown.MethodsUsing primary neurons from WIP‐defi… Show more

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Cited by 4 publications
(4 citation statements)
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“…Neuronal function and status are highly associated with neurite complexity, regulated through complex intracellular signaling events [ 35 , 36 ]. Therefore, we evaluated the neurite outgrowth pattern in terms of total neurite length, process number, and branch number in cultured cortical neurons.…”
Section: Resultsmentioning
confidence: 99%
“…Neuronal function and status are highly associated with neurite complexity, regulated through complex intracellular signaling events [ 35 , 36 ]. Therefore, we evaluated the neurite outgrowth pattern in terms of total neurite length, process number, and branch number in cultured cortical neurons.…”
Section: Resultsmentioning
confidence: 99%
“…Furthermore, stimulated by several growth factors the Akt-mTORC1-S6K pathway is involved in actin cytoskeleton reorganization (Jaworski and Sheng, 2006) and S6K promotes actin filament crosslinking and stabilization by directly binding F-actin, depending on the level of S6K phosphorylation (Moresco et al, 2005). WIP not only plays a cytoskeletal role, but also governs signaling through mTORC1-and Abl-dependent modulation of the S6K pathway, which controls neuritic extension and branching (Franco-Villanueva et al, 2015).…”
Section: Wip and Actinmentioning
confidence: 99%
“…We observed dysfunction of some Akt downstream elements in WIP-deficient neurons, although further work is needed to link mTORC1 dysfunction, F-actin polymerization and RhoA in these cells. [39][40][41] Many data support an essential role for WIP and GTPases, not only in tumor cell migration but also in cancer stem cell proliferation. These data allow the proposal of a molecular mechanism involved in cell proliferation, differentiation and actin cytoskeleton dynamics, all instrumental features in cell transformation and invasiveness.…”
Section: Future Perspectivesmentioning
confidence: 99%
“…The lack of WIP in hippocampal neurons co-cultured with astrocytes leads to increased dendritic spine size and Factin levels. 39,40 Identification of the molecular mechanism underlying this phenotype showed direct involvement of increasing amounts of the RhoA GTPase but not of Cdc42 or Rac1, whose levels appear to be normal. Absence of WIP produces a three-fold increase in RhoA levels as well as consistently higher RhoA activity and membrane-associated distribution.…”
Section: -Wip Exerts Opposite Roles In Neuronal Differentiation and Glioma Proliferationmentioning
confidence: 99%