In vivo evidence for mTORC2-mediated actin cytoskeleton rearrangement in neurons

Angliker, Nico and Rüegg, Markus A.. (2013) In vivo evidence for mTORC2-mediated actin cytoskeleton rearrangement in neurons. Bioarchitecture, 3 (4). pp. 113-118.

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Official URL: http://edoc.unibas.ch/53456/

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The mammalian target of rapamycin (mTOR) assembles into two distinct multi-protein complexes called mTORC1 and mTORC2. While mTORC1 controls the signaling pathways important for cell growth, the physiological function of mTORC2 is only partially known. Here we comment on recent work on gene-targeted mice lacking mTORC2 in the cerebellum or the hippocampus that provided strong evidence that mTORC2 plays an important role in neuron morphology and synapse function. We discuss that this phenotype might be based on the perturbed regulation of the actin cytoskeleton and the lack of activation of several PKC isoforms. The fact that PKC isoforms and their targets have been implicated in neurological disease including spinocerebellar ataxia and that they have been shown to affect learning and memory, suggests that aberration of mTORC2 signaling might be involved in diseases of the brain.
Faculties and Departments:05 Faculty of Science > Departement Biozentrum > Neurobiology > Pharmacology/Neurobiology (Rüegg)
UniBasel Contributors:Rüegg, Markus A.
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Taylor & Francis
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:18 Mar 2019 16:35
Deposited On:03 Oct 2017 08:19

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