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FSHN 470- Unit 1
| Question | Answer |
|---|---|
| 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
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