Phosphofructokinase-1 (PFK-1)
Cofactors used
Clinical / pharmacological. Tarui disease (GSD VII): exercise intolerance, haemolysis
What it does, reaction by reaction
Glycolysis Carbohydrate Metabolism · Cytosol
Fructose-6-phosphate + ATP -> fructose-1,6-bisphosphate + ADP
Converts Fructose-6-phosphate into Fructose-1,6-bisphosphate
› Notes
Phosphofructokinase-1 (PFK-1) uses ATP and Mg2+. This is the principal rate-limiting, committed, and irreversible step of glycolysis; fructose-1,6-bisphosphate is committed to glycolytic cleavage rather than glucose-6-phosphate-dependent alternative pathways.
Anaerobic Glycolysis / Lactic Acid Fermentation Energy Metabolism & Cellular Respiration · Cytosol
Fructose-6-phosphate + ATP → fructose-1,6-bisphosphate + ADP
Converts Fructose-6-phosphate ATP into Fructose-1,6-bisphosphate ADP
› Notes
Required cofactors: ATP and Mg2+. This is the pathway’s essentially irreversible, rate-limiting, and committed step of glycolysis; once fructose-1,6-bisphosphate is formed, the carbon is committed to glycolytic cleavage rather than glycogen synthesis or pentose phosphate flux.
Showing all 2 reactions.
What accelerates and inhibits it
Regulation is pathway-specific, so each context is listed separately
Anaerobic Glycolysis / Lactic Acid Fermentation
AMP, ADP, Pi, fructose-2,6-bisphosphate
ATP, citrate, low pH (H+) in muscle
Insulin activates hepatic PFK-2 activity, raising fructose-2,6-bisphosphate and PFK-1 flux; glucagon via PKA lowers fructose-2,6-bisphosphate in liver and inhibits glycolysis
Glycolysis
Listed there as: Phosphofructokinase-1
AMP, ADP, fructose-2,6-bisphosphate
ATP, citrate, low pH (especially muscle)
Insulin increases hepatic fructose-2,6-bisphosphate through dephosphorylated PFK-2/FBPase-2; glucagon lowers it via protein kinase A
Recent literature
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