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46 Cards in this Set
- Front
- Back
Feedback regulation
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In and ABCDE pathway once we get to a certain point in the pathway we are comitted to the end product. Feedback regulation is a way to prevent buildup of products.
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Phospfructokinase(PFK) regulation by AMP
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PFK is an enzyme that catalyzes the committed step in glycolisis.
The purpose of glycolysis is the generate ATP. An increase in the AMP concentration will feedback and stimulate PFK. ATP is an allosteric inhibitor of PFK |
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Compartmentation
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Into multienzyme comlexes or organelles is a way to regulate to environment or channel access of the enzyme to substrates
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Types of compartmentation
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Cytoplasm, mitochondria, lysosomes, ER(microsomes), golgu, peroxisomes, nucleus
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Coarse control
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Various ways of signalling the synthesis or degradatoin of enzymes. Could be transcriptional, translational, regulating modification, consititutive, inhibition, activation
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Fine control mechanisms
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Having a direct effect on enzymatic activity.
Protein/protein interactin, AA modification, allosteric regulation |
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cAMP protein dependent kinase
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A protein protein interaction that removes an inhibitor by phosporylating and the protein kinase can work
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Protein Kinase does
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It phosphorylates proteins in order to activate them
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Phosphatase
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dephosphorylates proteins in oder to deactivate them, this is good for recycling of proteins
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Aspartate carbamoyl transferase
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Good model for feedback control. Shows that the allosteric inhibitor looks nothing like the substrates. They act on completely different sites when one concentration is more than the other.
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Relaxed v. Tense states
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The R states sis where teh substrate wants to bind to the enzyme
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Homotropic
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Means there is no allosteric cooperation
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Hetertropic
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Inhibitor shifts the curve right whihcc indicates and increase in substrate to get to 1/2Vmax.
Activator will shift the curve left and decrease the amount of substrate to get to 1/2 Vmax |
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Simoidal kinetics
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The concerted model is what we use but the sequential model explains it better
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Allosteric modifications
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Homotropic - only activate the enzyme and it is a substrate
Hetertropic - has a different structure and can activate or inhibit the enzyme |
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Cooperativity
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The influence ligand binding has on subunit subunit interaactions
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Positive cooperativity
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One ligad enhances the affinity for subsequent ligands
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Negative cooperativity
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One ligand bound makes it harder for more to bind
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Plots for cooperativty of enzymes
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1/velocity plot shows no cooperativity as a straight line
Positive cooperativity is a curve, hyperbolic. |
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Kinetic v [s] plots
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Myoglobin is a hyperbolic curve for no cooperativity.
Hb is a sigmoidal curve for positive cooperativity Negative cooperativity is half that of a myoglobin curve |
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Hill plots for allosteric interactions
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Slope>1 = + coop
Slope<1 = - coop Slope = 1 = no coop |
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Enzyme regulation in blood coagulation cascades
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Zymogen activation is the on switch
It is a fine control mechanism Cleavage of the peptide bonds to activate symogen is irreversible in the blood circulation |
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2 pathways for coagulation
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Intrinsic and extrinsic. Both merge at factor X which then converts prothrombin to thrombin
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Extrinsic Pathway of coagulation
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Inititation of process
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Intrinsic pathways of coagulation
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Amplification of process
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Thrombun
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Catalyzes the conversion of fibrinogen to fibrin which forms the soft clots
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Protein cofactors and Ca
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Ca facilitates teh formation of multiple enzyme complexes and catalyzes the binding to the Gla protein
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Chelating agents
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EDTA and Carboxyglutamate(Gla), are compounds that make enzymes bind to metals
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Proteases and clotting
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Natural proteases are inhibited during this process in order to facilitate tissue repair
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Plaminogen and plasmin
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Eventually dissovle the clot once the wound is repaired through tPA.
Tissure factor VII is used in a brain anneurism |
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Three phases of hemostasis
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1. Procoagulation - cascading mechanisms for clot formation
2. Anticoagulation - inactivation of cofactors and inhibition of hydrolases 3. Fibrinolysis - dissolution pf the clot and regeneration of coagulation factors |
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2 initial phases of coagulation
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1. Extrinsic pathway causing thrombin formation and intrinsinc pathway amplifying the process
2. Platelet aggregation to relase of factors for caogulation and plug formation |
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Platelets cause the release of
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1. Serotonin(vasoconstrictor)
2. Growth factor(repairs BVs) 3. Factor V - cofactor to facto X 4. Factor VII - alpha subunit 5. Factor IV - 6. lipoproteins and ADP - facilitate platelet aggregatoin |
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Aspirin and blood clotting
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Aspiring is a COX inhibitor which inhibits the formation of prostaglandins from aracadonic acid. This means it slows inflammation
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Thromboxane and aspirin
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Thromboxane is a prostaglandin that promotes platelet aggregation, When aspirin is used you must keep a balance between these.
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Tissue Factor
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Released when a blood vessel breaks. Combines with factor VII to activate thrombin. Factor VII is always present in minute amounts in the blood and activation of this pathway causes amplification of this enzyme.
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Factor X
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Complexes with TF/FVII(extrinsic)
COmplexes with FIX/FVIII(intrinsic) Converts prothrombin to thrombin |
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Thrombin
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Converts fibrinogen to fibrin.
Activates F V,VII,VIII, XIII |
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FXIIIa
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Forms the hard clot with fibrin
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Hemophelia
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Deficiency in FVIII
No FVIII/FIX complex means no activate FX |
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Gla formation
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Formed with the interaction of vitamin K and Glu
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Vitamin K
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Cofactor that becomes oxydized during the Glu-Gla reaction.
It needs to be reduced to continue the process. Dicoumeral is a blood thinner that inhibits Vit K reductase. Warfarin is a rat poison that does the same thing. |
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TFPI(Tissue factor protein inhibitor)
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Single protein with 3 domanis that inhibits the extrinsic pathway. It binds TF, FVII, and FX to inhibit all of them.
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Heparin
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Enhances the inhibition of FX and thrombin and is a blood thinner
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Protein C
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Can destroy compounds of the coagulation process
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Final steps in coagulation
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If the protein cofactors are not carboxylated then there will be no function
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