RT Journal Article
T1 Glutamine, MTOR and autophagy: a multiconnection relationship.
A1 Bodineau, Clément
A1 Tomé, Mercedes
A1 Murdoch, Piedad Del Socorro
A1 Durán, Raúl V
K1 ASNS
K1 GABA-shunt
K1 MTORC1
K1 glutamine
K1 glutamoptosis
AB Cancer cells metabolize glutamine mostly through glutaminolysis, a metabolic pathway that activates MTORC1. The AMPK-MTORC1 signaling axis is a key regulator of cell growth and proliferation. Our recent investigation identified that the connection between glutamine and AMPK is not restricted to glutaminolysis. Rather, we demonstrated the crucial role of ASNS (asparagine synthetase (glutamine-hydrolyzing)) and the GABA shunt for the metabolic control of the AMPK-MTORC1 axis during glutamine sufficiency. Our results elucidated a metabolic network by which glutamine metabolism regulates the MTORC1-macroautophagy/autophagy pathway through two independent branches involving glutaminolysis and ASNS-GABA shunt.Abbreviations: αKG: alpha-ketoglutarate; AMPK: AMP-activated protein kinase; ASNS: asparagine synthetase (glutamine-hydrolyzing); GLUD/GDH: glutamate dehydrogenase; GLS: glutaminase; GOT1: glutamic-oxaloacetic transaminase 1; MTORC1: mechanistic target of rapamycin kinase complex 1; TCA: tricarboxylic acid.
YR 2022
FD 2022-04-26
LK http://hdl.handle.net/10668/19690
UL http://hdl.handle.net/10668/19690
LA en
DS RISalud
RD Apr 7, 2025