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Distinct functional outputs of PTEN signalling are controlled by dynamic association with ?-arrestins.


ABSTRACT: The tumour suppressor PTEN (phosphatase and tensin deleted on chromosome 10) regulates major cellular functions via lipid phosphatase-dependent and -independent mechanisms. Despite its fundamental pathophysiological importance, how PTEN's cellular activity is regulated has only been partially elucidated. We report that the scaffolding proteins ?-arrestins (?-arrs) are important regulators of PTEN. Downstream of receptor-activated RhoA/ROCK signalling, ?-arrs activate the lipid phosphatase activity of PTEN to negatively regulate Akt and cell proliferation. In contrast, following wound-induced RhoA activation, ?-arrs inhibit the lipid phosphatase-independent anti-migratory effects of PTEN. ?-arrs can thus differentially control distinct functional outputs of PTEN important for cell proliferation and migration.

SUBMITTER: Lima-Fernandes E 

PROVIDER: S-EPMC3155309 | biostudies-literature | 2011 Jun

REPOSITORIES: biostudies-literature

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The tumour suppressor PTEN (phosphatase and tensin deleted on chromosome 10) regulates major cellular functions via lipid phosphatase-dependent and -independent mechanisms. Despite its fundamental pathophysiological importance, how PTEN's cellular activity is regulated has only been partially elucidated. We report that the scaffolding proteins β-arrestins (β-arrs) are important regulators of PTEN. Downstream of receptor-activated RhoA/ROCK signalling, β-arrs activate the lipid phosphatase activi  ...[more]

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