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FSHN 470- Unit 1

QuestionAnswer
endergonic +ΔG
exergonic -ΔG
why is ATP hydrolysis coupled to non-equlibrium runs? to make it spontaneous, ATP is expensive so it's controlled
three types of kinetic controls Km, allosteric, apo-to-holo
RNA polymerase aka Pol II
vitamins and minerals can be ___ for trans factors ligands (allosteric)
direction of protein synthesis amino to carboxy
regulation at the RNA level (4) rate of transcription, RNA processing, RNA stability, translation rate
inhibition of HMG CoA reductase by cholesterol is an example of feedback repression (inhibition affects enzyme activity)
two other ways HMG coA reductase is regulated phosphorylation/dephosphorylation and ubiquitin degradation
what does IREBP do in low iron status? binds both TFr and F (inhibits translation of F, induces activation of TFr)
what does IREBP do in high iron status? Fe binds to IREBP, then cannot bind to IRE (for both F and TFr)
two degradation pathways autophagy, ubiquitin
sarcopenia may be related to what? overactive ubiquitin pathways
fatty acid synthase + control dimer of 6 enzymes + acyl carrier protein; all in one gene so compartmentalized this way
ACP acyl carrier protein: flexible arm that shuttles substrate between enzymes (coenzyme of panthothenic acid)
meat is ___% protein 20%
competitive inhibitors not in living systems; affect Km (drugs like Lipitor- competitively inhibits HMG coA reductase)
noncompetitive inhibitors bind to site other than active site; affects Vmax (allosteric effectors)
cumulative allosteric effects (3) additive, cooperative (sum of effects > than by themselves), concerted (need both OR one overrides the other)
phosphorylated target protein outcomes trans factor (activator or repressor); enzyme (increased or decreased activity)
hormones that inhibit adenylyl cyclase choline-type (acetylcholine, alpha adrenergics, angiotensin II, somatostatin
hormones that stimulate adenylyl cyclase epinephrine-type (glucagon, beta adrenergics, etc)
glucokinase Km 10 mM (halfway between fasted and fed states)
how much glucose metabolized by glucokinase in fasted vs fed states? 2x as much in fed (based on M-M kinetics)
why not hypoglycemia b/w meals? must have insulin present to let glucose into cells
type 2 hexokinase isozyme insulin dependent tissues (muscle, adipose, etc)
type 1 hexokinase isozyme insulin independent tissues (brain, erythrocytes, kidney)
hexokinase allosteric inhibition by its product glucose-6 phosphate
three mechanisms of control transcription (hours), covalent modification (minutes), allosteric control (seconds)
fasting PC and PEPCK transcriptional control increased expression (glucagon, cAMP)
feeding PC and PEPCK transcriptional control insulin increases phosphodiesterase (enzymes degraded)
minor allosteric controls of PFK AMP +, ATP -
minor allosteric controls of F 1,6 bis P'ase AMP -
two gluconeogenic tissues liver, kidney
gluconeogenic substrate basic rule >3 C's
why can't you convert acetyl coA to glucose? acetyl coA only has 2 carbons
which AA is not glucogenic? lysine (2 carbons)
where can AA enter pathways? most substrates (purvate, TCA cycle); enter both fasting and fed states with different outcomes
glucose and glycogen phosphorylase inhibits it allosterically
AMP and glycogen phosphorylase activates it allosterically
ADP vs AMP relative change muscle is more responsive to AMP than ADP
Calcium calmodulin and glycogen phosphorylase activates it allosterically
Explain 2 ways in which high fructose intake is lipemic enters after PFK (regulated); FK has a lower Km than GK
SREBP-related changes in transcription occur for all of the following except citrate lyase
how does IREBP modulate iron? binds to IRE in the transferrin receptor and stabilizes it
activation of glycogen phosphorylase cAMP, pKa, phosphorylates phosphatase kinase -> glycogen phosphorylase
insulin controls glucose entry by glut 4 recruitment
large delta G aka flux generating enzyme
OTC is not regulated by allosteric regluation
IREBP binds to IRE on mRNA (no iron bound to it)
Created by: melaniebeale