A researcher concludes that skeletal muscle PFK-2 by is not regulated by phosphorylation, also publishes that heart muscle PFK-2 is. In the heart phosphorylation of PFK-2 lead to what effect in researcher work?
a)↑ turnover PFK-2
b)↑ transcription PFK-2
c)↓ production of fructose 2-6bisphosphate
d)↑production of fructose 2-6bisphosphate
Well usually phosphorylation inhibits PFK2 so less F2,6BP will be produced right? So now this research says otherwise ,does it mean the opposite happens? But at the same time it doesn't say any thing about FBPase,phosphorylation activates it so still can lower F1,6BP !! Lol,I don't know biochem at all!
"B"
insulin works through map kinases and its controlling the transcription of PFK-2
yes less f2,6bp becos it would be converted to f6p inhibit glycolysis, lets wait for cardio tho
when phosphorylation of heart PFK-2--------activated--------------more fructose 2,6 bidp to stimulate PFK-1 in heart and also INC the glycolylytic RATE of the myocyte. PFK-2 accomplish it via AMP activated PK path ( MC seen in heart having hard time to generate ATP) or seen in INSULIN------ that high glucose scenario. Phosphorylation PFK-2 DOES NOT affect trasc OR turnover rate of the matter and nor play either in F-1,6bio.
what is the answer @cardio
*D* "phosphorylation of PFK-2"-> Enhanced/↑ production of fructose 2-6bisphosphate