Biochemistry: Regulation Of Enzymes

Front 1

Describe the regulation of cholesterol synthesis. What is the name of the enzyme responsible?

Back 1

very important to regulate cholesterol synthesis b/c cholesterol cannot be degraded in human. HMG-CoA Reductase is the enzyme responsible. Also regulated by Insulin and Glucagon

Front 2

Discuss the formation of HMG-CoA Reductase.

Back 2

Formed in the cytosol by Acetyl-CoA, which is normally found only in mitochondria. It is transported to cytosol when cholesterol synthesis is needed.

Front 3

Why is substrate availability a regulator for enzyme activity? What is velocity?

Back 3

The more substrate that is available, the faster a reaction will proceed (up to a max velocity). Velocity is product formation / time, or the rate of the rxn/enzyme.

Front 4

Discuss Product Inhibition, particularly for Hexokinase.

Back 4

enzyme is inhibited by the DIRECT product that it acts upon to make.

Example - Hexokinase phosphorylates glucose to make G-6-P, which then inhibits Hexokinase when its levels are high enough in the cell.

Front 5

Why do Allosteric Enzymes show a sigmoidal curve related to velocity and substrate concentration?

Back 5

Allosteric enzymes have several subunits and exhibit cooperative substrate binding between these subunits.

Front 6

Homotrophic Effect

Back 6

binding of one substrate molecule to one subunit of an allosteric enzyme enhances the binding of other substrates to other subunits

Front 7

Heterotrophic Effect

Back 7

used in feedback inhibition and feed forward activation

Front 8

Allosteric Feedback Inhibition

Back 8

Binding of a specific compound to the allosteric binding site can inhibit the regulatory enzyme of a pathway. The compound is often the end product of a pathway.

Front 9

Allosteric Feedforward Activation

Back 9

After a commiting step of a pathway is performed, the last enzyme of a pathway is activated.

Front 10

Is feedback inhibition performed by a homotrophic effector?

Back 10

No, by a heterotrophic effector.

Front 11

Does fructose-1,6-bisphosphate allosterically activate or inhibit pyruvate kinase?

Back 11

Fructose-1,6-bisphosphate is formed by phosphofructokinase, and is the committed step of glycolysis. This feed-forward activates the enzyme Pyruvate Kinase.

Front 12

Discuss enzyme induction by insulin.

Back 12

Insulin signals high blood glucose levels and induces the liver to perform protein synthesis for key enzymes, to perform fatty acid synthesis, and to perform cholesterol synthesis.

Front 13

Discuss enzyme induction by glucagon.

Back 13

Glucagon signals low blood glucose levels and induces in the liver key enzymes for gluconeogenesis.

Front 14

Discuss phosphorylation / dephosphorylation as methods of covalent enzyme modification?

Back 14

phosphorylation typically inaxctivates an enzyme, while DEphophorylation activates enzymes.

Front 15

Do Protein Kinases and Phosphatases catalize irreversible reactions? Is the regulation reversible?

Back 15

The enzymes do indeed catalize irreversible reactions in that a kinase can only add a phosphate, but cannot remove it. A phosphotase must remove the phosphate group. The regulation, however, is reversible, because a phosphate group can be easily removed and the original form can be restored.

Front 16

Does Insulin or Glucagon lead mainly to phosphorylated key enzymes?

Back 16

Glucagon

Front 17

Which hormone induces HMG-CoA Reductase?

Back 17

Insulin

Front 18

Why would high AMP levels lead to phosphorylation of HMG-CoA Reductase. Compare to cAMP system.

Back 18

HMG-CoA Reductase is activated by substrate availability. After big, carb heavy meals, the enzyme is active. However, high AMP Levels suggest low ATP (cellular energy) levels. In this case, the enzyme is phosphorylated and inactivated.

Front 19

What is the message signaled to the liver by glucagon?

Back 19

Glucagon signals to the liver to begin gluconeogenesis and to stop fatty acid and cholesterol synthesis.

Front 20

How does glucagon perform hormonal regulation of HMG-CoA Reductase?

Back 20

Glucagon signals via its secondary messenger system to the liver to begin gluconeogenesis and to stop fatty acid and cholesterol synthesis. It also leads to the phosphorylation of HMG-CoA Reductase, thus inactivating it.

Front 21

Which cells have glucagon receptors? Where are these cells located?

Back 21

I don't fucking know!

Front 22

Name two actions of cholesterol on HMG-CoA Reductase?

Back 22

1. Inhibits transcription of HMG-CoA Reductase
2. Leads to accelerated degradation of HMG-CoA Reductase.