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This rapid and strong inhibition is critical to unleash autophagy, which in turn boosts free amino acid levels that feed gluconeogenesis to sustain glycaemia ( RagA (RagA Q66L , referred to as RagA GTP ) that renders mTORC1 constitutively active regardless of nutrient levels are unable to trigger autophagy after birth, suffer a profound hypoglycemic state they do not recover from, and finally succumb within 1 day after birth ( Sestrin 1, 2 and 3 , negative regulators of the Rag GTPases ( Atg5 / ( Atg7 / mice (Table 1)

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