TCA's reg & connection to PDHC reg Flashcards
ETC-OCPHOS
req tight coupling of the use of O2, because it is the terminal e- acceptor. If last e- acceptor, must have enough O to be able to do this. (to exit ETC)
NADH must be re-ox, because it will inject e- into ETC (enter ETC)
ATP synthesis: this is the ox-phos part, made ATP and sends it to the ETC
TCA makes…
NADH, so TCA coordinates amount of NADH with amount of ATP needed bc TCA, ETC. Ox-PHOS which are all coupled.
CS
citrate synthase originally thought to be controlled by concentration of OA affecting amount of citrate produced.
How does this link to previous info?
Lagre delta G, but this enzyme operates close to equilibrium (cellular conditions diff from standard).
Means: OA is still going to control by substrate availability… delta G is not as big as we thought…
Big E drop cannot be paid by CS
control points
IDH (isocitrate DH) and a-KGDH, are the control points, which are inhibited with isocitrate being the major point (like with PFK1)
Succinyl-CoA and NADH
CoA is a larger part of the molecule, succ is small (only 4 C).
These two are CI of a-KGDH…
NADH is CI of E2 and inhibits a-KG binding to E1.
a-KGDH affinity
ADP, Pi, and Ca2+ increase E1’s a-KG affinity, kind of similar to PDHC… but a-KGDH doesnt have cov modifier.
; ATP inhibits by opposing ADP’s activity… two diff but related allosteric effectors, one opposing the other.
How/where/why for IDH and a-KGDH
How: CI or something
where:
why : either have a lot of E or not a lot of E.
PFK1 and 2 are both inhibited by cit
means:
if glyc inhibited and the flux controller, dont want to ber unning glycolysis. Getting E from somewhere else or have enough E