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Literature summary for 2.7.1.1 extracted from

  • Roberts, D.J.; Tan-Sah, V.P.; Ding, E.Y.; Smith, J.M.; Miyamoto, S.
    Hexokinase-II positively regulates glucose starvation-induced autophagy through TORC1 inhibition (2014), Mol. Cell, 53, 521-533.
    View publication on PubMedView publication on EuropePMC

Protein Variants

Protein Variants Comment Organism
F199A mutation in mTOR signaling motif. While overexpressed wild-type enzyme associates with mTOR and raptor, mutant F199A does not show association above control levels Rattus norvegicus

Organism

Organism UniProt Comment Textmining
Rattus norvegicus P27881
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Source Tissue

Source Tissue Comment Organism Textmining
cardiomyocyte ventricular myocyte Rattus norvegicus
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Synonyms

Synonyms Comment Organism
hexokinase-II
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Rattus norvegicus

General Information

General Information Comment Organism
physiological function inhibition of hexokinase-II diminishes, while overexpression of hexokinase-II potentiates autophagy induced by glucose deprivation in cardiomyocyte and noncardiomyocyte cells. Hexokinase-II binds to and inhibits the autophagy suppressor, mTOR complex 1 (TORC1), and this binding is increased by glucose deprivation. Mutating the TOS motif, a scaffold sequence responsible for binding TORC1 substrates, in hexokinase-II blocks its ability to bind to TORC1 and regulate protective autophagy. The transition from glycolysis to autophagy appears to be regulated by a decrease in glucose-6 phosphate Rattus norvegicus