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While this regulation is entirely independent of mTORC1 (Arsham et al., 2002), in response to upstream growth factors and oncogenes, activation of mTORC1 stimulates an increase in HIF1α via enhanced cap-dependent translation of the HIF1 a mRNA, which is sufficient to stimulate an increase in glucose uptake and glycolysis even when oxygen is not limiting (e.g
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Zhang K, Xu P, Sowers JL, Machuca DF, Mirfattah B, Herring J, et al
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