Glycolysis & PFK1/F1,6BPase

Question	Answer
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)

Resource summary

	Created by gina_evans0312 over 10 years ago