MassIVE MSV000079671

Partial Public PXD004024

MITOCHONDRIAL Akt REGULATION OF HYPOXIC METABOLIC REPROGRAMMING

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Description

Hypoxia is a driver of aggressive tumor behavior, but the mechanisms are not completely understood. In a global phosphoproteomics screen, we now demonstrate that hypoxia induces the recruitment of Akt2 to tumor mitochondria, and Akt phosphorylation of pyruvate dehydrogenase kinase (PDK1) on Thr346. In turn, Akt-phosphorylated PDK1 shuts off oxidative phosphorylation via phosphorylation of the pyruvate dehydrogenase complex, and reprograms tumor metabolism towards glycolysis. Akt-phosphorylation of PDK1 is required to prevent autophagy, maintain cell viability and support tumor cell proliferation in hypoxia, in vivo. Therefore, mitochondrial Akt is a pathophysiologic switch for tumor adaptation in hypoxia. [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: LC-MS/MS ; SILAC ; Phosphoproteome ; Akt ; Mitochondria

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Principal Investigators:
(in alphabetical order) 		Dario C. Altieri
Submitting User: tangh
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