exam 5 Flashcards
what is the committed step of purine biosynthesis
PRPP to 5 phospho-B-D-ribosylamine
PRPP glutamyl transferase
amido transferase
how is the committed step of purine biosynthesis regulated
positive = PRPP negative = product inhibion like IMP,GMP, AMP
for the committed step of purine biosynthesis how does alpha of ribosyl get inverted to beta
Mechanism is SN2 so the nucleophine (amino group)must attack at the opposite face of the leaving group resulting in a switch from alpha to Beta
why is ATP not required in committed step of purine biosynthesis
no activated intermediate because we have a good leaving group
drug inhibits adenylate cyclase which makes cAMP
2 groups one with and wihtout drug and both no food for 8 hours who has lower blood glucose
drug treated
drug inhibits adenylate cyclase which makes cAMP
2 groups one with and wihtout drug and both no food for 8 hours upon what organ is the drug accting
liver
drug inhibits adenylate cyclase which makes cAMP
2 groups one with and wihtout drug and both no food for 8 hours
pathway of organ, treatment alteration, downstream effect
inhibits the activation of glycogen breakdown by inhibiting adenylate cyclase
usually when fasting glucagon ->activated g protein to activated adenylate cyclase (drug inhibition here) to increased cAMP to activated pKA which will both phosphorylate phosphoylase kinase to phosphoyrlate phosphoyrlase to activate glycogen break down and phosphorylate glycoge synthase to inactivate it
so the drug blocks the downstream effect of inhibiting glycogen synthase and activating glycogen phosphorylase
HOW DOES THIS REDUCE BLOOD GLUCOSE
role of malate/aspartate shuttle
restores NADplus to the cytosol
is the malate/aspartate shutttle more impoortant for aerobic or anarobic conditions
aerobic conditions because in anaerobic conditions the conversion of pyruvate to lactate maintains NADplus in cytosal for glycolysis to continue
reciperocal regulated
one path is inhibited while other is activated
why RR glycolysis and gluconeogensisis
GLycolysis generates energy but gluconeogenisis requires energy so it would be wasteful to use simultaneously
signal for RR glycolysis and gluconeogenesis
F-2-6-BP activates glycolysis by stimulateing PFK1 activiety to increase conversion of f6P to F16B2
F26BP inhibits gluconeogenisis by negatively regulating F16BP which inhibits the conversion of F16BP to F6P
pyruvate dehydrogenase consists of a highly organized supramolecular complex containgig multiple copies of each of three enYems that are arranged with one type in aninteral cluster with two types in oustide clusters
true
composed of 3 enzymes E1-3
E1 and E3 are outside so they can pick up substrate (pyruvate) and release products(acetylu CoA, CO2 and NADH)
coenzyme co-substrates that are non-covalently attatched to pyruvate dehydrogenase include NAD+ and Coenzyme A
NAD+ = E3 co-enzyme cosubstrate and Coa = E2 co co
TPP for E1 and lipoamide for E2 and FAD for e3 are all prosthetic groups
NADH but not acetyl CoA is a competitive and an allosteric regulator of specific enYmes fo rPDH supramolecular complex
false
acetyl CoA is a negative regulator of PDH
all steps of TCA are energetically favorable
false
only a few steps are E favorable but have large enough -deltaG to push the cycle forward
coordinated allosteric regulation of TCA cycle by ADP and ATP occur at specific enzymatic steps, in which neither of these molecules resemble eihter the substrate or producet
ture
ATP and ADP are allostereic regulators of the TCA cycle enyzyme IDH
the electron transport chain provides 2 specific substrates for TCA
true
NAD+ and FAD
Assymetrically oriented (anisotorpic localization of COmplexes I-IV in mitochondrial is not importatnt for oxidative phospohyorlation
false
assymetric orientation of complexes is imiportant to ensure H+ being pumped in same direction (to inner membrane) for each complex
Complexes I-IV are separable sucha that each can function independently of each other but some of these complexes can also be found associated together suggesting higher level of organization of ETC system
true
III-IV complexe demonstrated
the electrochemical gradient formed by the electron transport chain is necesssary to drive the binding change mechanism of ATP syntessis in oxidative phosphorylateion
true
movement of H+ down its gradient establishe dby ETC provides energy for ATP synthesis
c irng to delta to beta?
a myocardial infarction is known to cause a decrease in the suply of oxygen to circulation and ultimatly mitochondria
what are the impacts
decrease in rate of ATP synthase
increase the rate of proton pumpin gcomplex IV
because the reduction of O2 is the final step in the ETC, so teh ETC (and thus rate of H+ pumping) will decrease
ATP syntheiss is couple to the ETC so it will decrease too
P:O ratio
close to 3 when NADH is electron source for ETC
refers to the moles of ATP produced per .5 moles of O2 reducted by C IV using electron frsom either FADH2 or NADH
it depends on the difference in oxidation-reduction potential and intial electron donor and ultimate electron acceptor in ETC
the P:O ratio describes the relationship between moles of ATP produce and half moles of O 2 reduced
it is 3 for NADH but 1.8 for FADH2 because it bypasses C I
protein component of ATP synthasome
where
how many
binding to proton from the gradient produced by ETC
C-ring subunit of FO domain
located in inner membrane, 1 c ring w/ 10-14 subunits
