PFK-1, FBPase-1, F26P and 2nd substrate cycle

Question 1

F26P is a key regulator in…

Answer 1

mammals.
- not a metabolite in either pathway (GNG or glycolysis), made by a shunt which is an offshoot from a pathway
- strong allosteric activator of PFK-1 and inhibitor of FBPase-1, which means more glycolysis flux abd inhibits GNG flux (metabolites)
- F26P control systems vary by tissue
- only need a small [F26P] to be able to do this

Question 2

If glucagon high

Answer 2

low blood sugar, which will activate PKA, which will phosphorylate a ser on flux controller’s PK2 (PFK2/FBPase2 - which makes or breaks F26P)

If PFK2 is phosphorylated, FBPase-2 is active, then we stop phosphorylating the reactant to give a product (F6P to F26P will not occur, instead FBPase-2 take F26P to make F6P which can reenter glyc or GNG)

Question 3

If insulin high

Answer 3

Affects Protein phosphatase,PP2A, by causing the removal of the added phosphate to activate PFK-2 and inhbit FBPase-2.
Now the dephospho enzyme will phoshphorylate the reactant to create the phosphorylated product (F6P to F26P occurs)