Topic
Glycolysis
About: Glycolysis is a research topic. Over the lifetime, 10593 publications have been published within this topic receiving 507460 citations. The topic is also known as: GO:0006096 & glycolysis.
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TL;DR: The study of oscillations reveals the dynamics of a pathway over a large range of states and an implicit function of their feedback structure, which involves cross-coupling and self-Coupling with opposite sign in a two variable structure and might produce kinetic instability involving more than one singularity of the trajectories in a phase plane.
324 citations
TL;DR: Changes in oxidative capacity directly influence the sensitivity of cytosolic respiratory control and this, in turn, has important consequences for maintenance of cellular energy balance.
324 citations
TL;DR: Inhibition of PGAM1 by shRNA or a small molecule inhibitor PGMI-004A results in increased 3-PG and decreased 2-PG levels in cancer cells, leading to significantly decreased glycolysis, PPP flux and biosynthesis, as well as attenuated cell proliferation and tumor growth.
324 citations
TL;DR: Overall, it is demonstrated how extracellular fluxes quantitatively reflect intracellular ATP turnover and cellular bioenergetics.
322 citations
TL;DR: Inhibiting the FKBP12/rapamycin-sensitive subset of mTOR functions in leukemic cells enhanced aerobic glycolysis and decreased uncoupled mitochondrial respiration within 25 min, as shown by the synergy between the glycoleytic inhibitor 2-deoxyglucose and rapamycin in decreasing cell viability.
Abstract: mTOR is a central regulator of cellular growth and metabolism. Using metabolic profiling and numerous small-molecule probes, we investigated whether mTOR affects immediate control over cellular metabolism by posttranslational mechanisms. Inhibiting the FKBP12/rapamycin-sensitive subset of mTOR functions in leukemic cells enhanced aerobic glycolysis and decreased uncoupled mitochondrial respiration within 25 min. mTOR is in a complex with the mitochondrial outer-membrane protein Bcl-xl and VDAC1. Bcl-xl, but not VDAC1, is a kinase substrate for mTOR in vitro, and mTOR regulates the association of Bcl-xl with mTOR. Inhibition of mTOR not only enhances aerobic glycolysis, but also induces a state of increased dependence on aerobic glycolysis in leukemic cells, as shown by the synergy between the glycolytic inhibitor 2-deoxyglucose and rapamycin in decreasing cell viability.
320 citations