Creado por gina_evans0312
hace más de 10 años
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Pregunta | Respuesta |
Function of Glycolysis | Provides ATP from glucose, Acetyl CoA for FA synthesis, and carbon skeletons for aa sythesis |
In Muscle, glycolysis and gluconeogenesis are | Simultaneous, as one feeds the other |
In liver, glycolysis and gluconeogenesis are... | Incompatable- glucose produced must exit the liver to be used elsewhere |
Glycolysis Regulation | Control glucose entry (GLUT2) or at committed steps |
PFK1 | 6- Phosphofructokinase 1 (the first committed enzyme) converts Fru-6-P to Fur-1,6-BP |
PFK1 Structure | Tetramer, with tense (active) and relaxed (inactive) form |
PFK1- ATP Binding | 2 sites- one allosteric, one catabolic (binds regardless of tense/relaxed state) |
PFK1- Allosteric ATP | Excess ATP binds and encourages tense state (indicated energy dense cell) |
PFK1- F-6-P binding | Only occurs in relaxed state |
PFK1- Allosteric AMP | Competes with ATP in low ATP concs, encouraging relaxed state |
PFK1- H+ ions | Indicate high levels of anaerobic respiration and so PFK1 is shut down for cellular protection |
Heart PFK1- H+ ions | Even in high H+ concs, heart PFK1 remains active as shutting it down is potentially fatal |
PFK1- Citrate | Inhibits PFK1 (Signals TCA cycle overload) |
PFK1- F-6-P Signals | Glucose entry/breakdown, acts as feedforward mechanism |
PFK1- F-2,6-BP | Potent allosteric activator |
F-1,6-BPase | Reverses action of PFK1 (though PFK1 works 10x faster) |
Active F-1,6-P Location | Muscles undergoing gluconeogenesis |
F-1,6-P - AMP | At low AMP, F-1,6-P activity exceeds that of PFK1 (this reverses as AMP levels rise) |
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