Exam 1 Flashcards
2009
The ΔG’º for hydrolysis of ATP is -30.5 kJ/mole. The ΔG’º for hydrolysis of PEP is -61.9 kJ/mole. The ΔG’º for the following reaction is:
PEP + ADP ⇔ Pyruvate + ATP
- -92.4 kJ
- +31.4 kJ
- -31.4 kJ
- +92.4 kJ
- cannot be determined from data provided
-31.4 kJ
( -61.9 - (-30.5) = -31.4 )
2009
For A ⇔ B, ΔG’º is negative.
- The rate of reaction of B to A is increased
- The rate of reaction of B to A is decreased
- The rate of reaction of B to A is dependent on the magnitude of ΔG’º
- The rate of reaction is not influenced by the sign of magnitude of ΔG’º
- There is no reaction at all in either direction becase it is at equilibrium
The rate of reaction is not influenced by the sign of magnitude of ΔG’º
2009
ln K (K equilibrium constant) is equal to
- RT ΔG’º
- RT ΔG’º
- ΔG’º/RT
- ΔG’º/RT
- ΔG’ºT/R
- ΔG’º/RT
( ΔG’º = -RT ln K)
2009
ΔG’º (under cellular conditions) for ATP hydrolysis is -50 kJ/mole and 4000 kJ our caloric intake (in 24 hours) is used for synthesis ATP. The amount of ATP formed by a human in 24 hours is (MW ATP ≈ 500)
- ≈ 6g
- 80g
- 0
- -40 Kg
- ATP is only hydrolized
-40 Kg
2009
In glycolysis ATP synthesis is catalyzed by
- 6-phosphofructo-1 kinase
- hexokinase
- phosphoglycerate kinase
- glyceraldehyde 3-phosphate dehydrogenase
- none of the above
phosphoglycerate kinase
2009
The irreversible reactions of glycolysis include that catalyzed by
- phosphoglycerate kinase
- fructose biphosphate aldolase
- 6-phosphofructo-1-kinase
- glyceraldehyde 3-phosphate dehygrogenase
- phosphoglucose isomerase
6-phosphofructo-1-kinase
2009
6-Phosphofructo-1-kinase activity can be decreased by all of the following EXCEPT
- low pH
- AMP
- decreased concentration of fructose 2,6-bisphosphate
- ATP at high concentrations
- citrate
AMP
2009
Which of the following supports gluconeogenesis?
- lysine degradation
- leucine degradation
- acetyl CoA + oxaloacetate + H2O ⇔ citrate + CoA
- pyruvate + ATP + HCO3 ⇔ oxaloacetate + ADP + Pi + H+
- α-ketoglutarate + aspartate ⇔ glutamate + oxaloacetate
pyruvate + ATP + HCO3 ⇔ oxaloacetate + ADP + Pi + H+
2009
In the Cori Cyle
- glucose is converted to pyruvate/lactate in anaerobic (i.e. red blood cells) tissues, and this pyruvate/lactate return to the liver, where it is converted to glucose
- nitrogen from alanine must be converted to urea, increasing the amount of energy required to drive the process
- only tissues with aerobic metabolism (i.e. mitochondria and O2) are involved
- the same amount of ATP is used in the liver to synthesize glucose as it is released during glycolysis, leading to no net efect on whole-body energy balance
- a three-carbon compound arising from glycolysis is converted to glucose at the expense of energy from fatty acid oxidation
glucose is converted to pyruvate/lactate in anaerobic (i.e. red blood cells) tissues, and this pyruvate/lactate return to the liver, where it is converted to glucose
2009
Gluconeogenic enzymes include all of the following EXCEPT
- phosphoenolpyruvate carboxykinase
- pyruvate carboxylase
- fructose 1,6-bisphosphatase
- phosphogucmutase
- glucose 6-phosphatase
phosphogucmutase
(only in glycolysis)
2009
Phospho-dephospho regulation of, 6-phosphofructo-2-kinase, and pyruvate kinase is an important regulatory mechanism in
- skeletal muscle
- liver
- intestine
- erythrocytes
- brain
liver
(where glycolysis occurs)
2009
Phosphorylation-dephosphorylation and allosteric activation of enzymes play roles in stimulating glycogen degradation. All of the following result in enzyme activation EXCEPT
- Phosphorylation of Phosphorylase kinase
- Phosphorylation of protein kinase A
- binding of AMP to Phosphorylase b
- Phosphorylation of Phosphorylase
- dePhosphorylation of glycogen synthase
Phosphorylation of protein kinase A
2009
Glucose 6-phosphatase, which is deficient in Von Glerke’s disease, is necessary for the production of blood glucose from
- fructose
- galactose
- amino acid carbon chains
- liver glycogen
- all of the above
all of the above
2009
Glucose labeled at C-1 is incubated with glycolytic enzymes and necessary cofactors. The pyruvate CH3COCOO- that is formed will be labeled at
- C-1
- C-2
- C-3
- All C atoms
- At none of the C atoms
C-3
2009
Removal of a glucose residue from glycogen (by phosphorylase) and passing it thorugh glycolysis to 2 pyruvates yields _____ ATP
- 1
- 2
- 3
- 4
- None
3
2009
Glucose labeled at C-3 is allowed to undergo fermentation to ethanol CH3CH2OH and CO2. The label will show in
- Ethanol at C-1 only
- Ethanol at C-2 only
- CO2 only
- Both A and C
- Both B and C
CO2 only
2009
The conversion of 1 mol of fructose 1,6-biphosphate to 2 mol of pyruvate by the glycolytic pathway results in a net formation of:
- 2 mol of NADH and 2 mol of ATP
- 1 mol of NADH and 1 mol of ATP
- 2 mol of NADH and 4 mol of ATP
- 1 mol of NAD+ and 2 mol of ATP
- 2 mol of NAD+ and 4 mol of ATP
2 mol of NADH and 4 mol of ATP
2009
Which of the following statements is true of muscle glycogen phosphorylase?
- It removes glucose residues from the reducing ends of the glycoen chains
- It exists in an active (a) form and an inactive (b) form that is allosterically regulated by AMP
- It degrades glycogen to form glucose 6-phosphate
- It catalyzes phosphorolysis of the α(1→6) bonds at the branch points of glycogen
- It degrades glycogen to glucose
It exists in an active (a) form and an inactive (b) form that is allosterically regulated by AMP
2009
Which of these enzymes is a control point, regulated by the cell’s energy supply?
- Phosphofructokinase-1
- Glycogen phosphorylase
- Pyruvate kinase
- All of the above are control points
- None of the above is a control point
All of the above are control points
2009
The main function of the pentose phosphate pathway is to
- Supply pentoses and NADPH
- Give the cell an alternate pathway should glycolysis fail
- Supply NADH
- Provide a mechanism for the utilization of the carbon skeletons of excess amino acids
- Supply energy
Supply pentoses and NADPH
2009
Which of the following describes fatty acid transport into the mitochondrial matrix?
- It is the rate-limiting step in fatty acid oxidation
- It is regulated by malonyl-CoA
- The cytosolic and matrix pools of CoA are distince and separate
- Once fatty acyl groups have entered the matrix, they are committed to oxidation to acetyl-CoA
- All of the above are true
All of the above are true
2009
Fatty acid synthase of mammalian cells
- uses a four-step sequence to lengthen a growing fatty acyl chain by one carbon
- contains ACP, which carries acyl groups attached through thioester linkages
- requires chemical energy in just one form, the reducing power of NADPH
- is activated by glucagon and epinephrine
- is activated by palmitoyl CoA, the principal product of fatty acid synthesis
contains ACP, which carries acyl groups attached through thioester linkages
2009
How are fatty acid oxidation and synthesis controlled so that futile cycling (when two opposing reactions/pathways occurring in the same location and at the same time, one forming an energy-rich compound, the other consuming an energy-rich compound) does not occur?
- A - they occur in different cellular compartments
- B - they employ different electron carriers
- C - the product of the first oxidation reaction inhibits the rate-limiting step of biosynthesis
- A and B
- A, B, and C
A and B
2009
In mammmalian cells, fatty acid synthesis occurs in the cytosol. The beginning subsrate for this series of reaction is acetyl-CoA, which is formed in the mitochondrial matrix. How does the acetyl-CoA move from matrix to cytosol?
- Acetyl-CoA reacts with oxaloacetate and leaves the matrix as citrate via the citrate transporter
- Acetyl-CoA combines with bicarbonate and is transported out of the matrix as pyruvate
- There is a specific transport protein for acetyl-CoA
- Acetyl-CoA is a nonpolar molecule and can diffuse across all membranse
- Inner and outer mitochondrial membranes are freely permeable to Acetyl-CoA due to the presence of transmembrane pore or channels.
Acetyl-CoA reacts with oxaloacetate and leaves the matrix as citrate via the citrate transporter
2010
Which of the following BEST describes the relationship between ΔG and the rate of a reaction?
- ΔG is linearly proportional to the rate
- ΔG is inversely proportional to the rate
- if ΔG > 0, the reaction is spontaneous
- if ΔG < 0, the reaction is at equilibrium
- ΔG provides no information about the rate
ΔG provides no information about the rate
2010
For the reaction A → B, the Keq is 104. If a reaction mixture originally contains 1 mmol of A and no B, which of the following is true? (R = 8.32 J mol-1K-1, T = 300ºK)
- At equilibrium, there will be far more A than B
- The reaction will definitely proceed toward B at a very high rate
- ΔGº’ for the reaction will be large and positive
- The rate of the reaction may be immeasurably small
- ΔGº’ will be approximately -23kJ/mole
2010: ΔGº’ will be approximately -23kJ/mole
2012, 2015: A. At equilibrium, there will be far more B than A
2010
In a skeletal muscle cell ΔGº’ for hydrolysis of ATP to ADP + Pi is -50 kJ/mole. The approximate ratio of [ATP]/ADP][Pi] found in the cells at 37°C is ΔGº’ for ATP hydrolysis -30.5 kJ/mole, R = 8.32 J mol-1K-1
- 5000/1
- 4000/1
- 2000/1
- 1000/1
- 200/1
2000/1
2010
Glucose 1-phosphate is converted to fructose 6-phosphate in two successive reactions?
Glucose-1-P → glucose-6-P ΔG’º = -1.7 kcal/mol
Glucose-6-P → fructose-6-P ΔG’º = -0.4 kcal/mol
What is ΔG’º for the overall reaction?
- -2.1 kcal/mol
- -1.7 kcal/mol
- -1.3 kcal/mol
- 1.3 kcal/mol
- 2.0 kcal/mol
-2.1 kcal/mol
2010
The E0’ of the NAD+/NADH half reaction is -0.32 V. The E0’ of the oxaloacetate/malate half reaction is -0.175 V. When the concentrations of NAD+, NADH, oxaloacetate, and malate are all 10-5 M, the spontaneous reaction is:
- NAD+ + oxaloacetate → NADH + H+ + malatate
- NAD+ + NADH + H+ → malatate + oxaloacetate
- malatate + NADH + H+ → oxaloacetate + NADH + H+
- malatate + NAD+ → oxaloacetate + NADH + H+
- oxaloacetate + NADH + H+ → malatate + NAD+
oxaloacetate + NADH + H+ → malatate + NAD+
2010
A person who cannot synthesize liver fructose 1,6-biphosphate would probably not be able to
- Synthesize fats when the diet contained excess carbohydrate
- Metabolize fructose
- Convert fructose 1,6-biphosphate into triose phosphates
- Resynthesize glucose from lactate produced during exercise
- None of the above are correct
Resynthesize glucose from lactate produced during exercise
2010
glucose can not be synthesized from which of the following noncarbohydrate precursors?
- fumarate
- alanine
- lactate
- palmitic acid
- glycerol
palmitic acid
2010
Starting from a glucose residue in glycogen, how many net ATP molecules will be formed in the glycolysis of the residue to pyruvate?
- 1
- 2
- 3
- 4
- 5
3
2010
If the C-1 carbon of glucose were labeled with 14C, which of the carbon atoms in pyruvate would be labeled after glycolysis?
- The carboxylate carbon
- The carbonyl carbon
- The methyl carbon
- none
- all carbon atoms will be labeled
The methyl carbon
2010
Phosphofructokinase activity is enhanced by which of the following?
- Increased ATP concentration
- Increased fructose 2, 6-biphosphate concentration
- Increased citrate concentration
- Decreased AMP concentration
- Increased [glucagon] serum
Increased fructose 2, 6-biphosphate concentration
2010
Place the following steps of the reaction cascade of glycogen metabolism in the proper sequence
- activation of protein kinase
- formation of cyclic AMP by adenylate cyclase
- phosphorylation of phosphorylase kinase
- hormone binding to target cell receptors
- phosporylaiton of glycogen synthase a and phosphorylase b
- 1,2,3,4,5
- 2,4,1,5,2
- 4,2,1,3,5
- 5,4,3,2,1
- 2,1,4,5,3
4,2,1,3,5
2010
Inorganic fluoride inhibits enolase. In an anaerobic system that is metabolizing glucose as a substrate, which of the following compounds would you expect to increase in concentration following the addition of fluoride?
- glucose
- phosphoenolpyruvate
- glyoxylate
- 3-phosphoglycerate
- pyruvate
3-phosphoglycerate
2010
The conversion of one mole of glucose-6-phosphate to two moles of lactate in glycolysis is accompanied by a net gain of:
- 3 moles of ATP
- 2 moles of ATP
- 1 mole of ATP
- 1 mole of NADH
- 2 moles each of ATP and NADH
3 moles of ATP
2010
In glycolysis, fructose 1,6-biphosphate is converted to two products with a standard free-energy change (ΔG°’) of 23.8 kJ/mol. Under what conditions encountered in a normal cell will the free-energy change (ΔG°’) be negative, enabling the reaction to proceed spontaneously to the right?
- 2010 / 2015: Under standard conditions, enough energy is released to drive the reaction to the right
- 2010 / 2015: The reaction will not go to the right spontaneously under any conditions because the ΔG°’ is positive
- 2010 / 2015: The driving force of this reaction is supplied by a coupled exergonic reaction, the hydrolysis of ATP
- 2015: When there is a high concentration of products relative to the concentration of fructose 1,6- bisphosphate.
- 2010: The reaction may proceed given appropriate concentrations of fructose-1,6-bisphosphate and the products
- 2015: When there is a high concentration of fructose 1,6-bisphosphate relative to the concentration of products
- 2010 / 2015: none of the above conditions is sufficient
- 2010: The reaction may proceed given appropriate concentrations of fructose-1,6-bisphosphate and the products
- 2015: When there is a high concentration of fructose 1,6-bisphosphate relative to the concentration of products
2010
If glucose labeled with 14C in C-3 were fed to yeast carrying out of the ethanol fermentation, where would the 14C label be in the products?
- C-1 (methyl group) of ethanol
- C-1 of ethanol only
- CO2 only
- C-2 of ethanol and CO2
- C-1 of ethanol and CO2
CO2 only
2010
Glyceraldehyde-3-phosphate labeled with 14C in C-1 (the carbonyl carbon) is mixed wiht unlabeled dihydroxyacetone phosphate and the enzymes triose phosphate isomerase and aldolase. After a period of incubation, fructose-1,6-bisphosphate is isolated from this system. It will be labeled with 14C in:
- C-1 only
- C-3 only
- C-1 and C-3
- C-1 and C-6
- C-3 and C-4
C-3 and C-4
2010
Galactosemia is a genetic error of metabolism principally associated with
- excessive ingestion of galactose
- inability to digest lactose
- deficiency of galactokinase
- deficiency of UDP-glucose: galactose 1-phosphate uridylyltransferase
- deficiency of UDP-glucose epimerase
deficiency of UDP-glucose: galactose 1-phosphate uridylyltransferase
2010
When blood glucose levels are low, glucagon is secreted. Which of the following are the effects of increased glucagon levels on glycolysis and related reactions in the liver?
- Phosphorylation of phosphofructokinase 2 occurs
- Dephosphorylation of phosphofructokinase 2/fructose bisphosphatase 2 occurs
- phosphofructokinase-1 is activated
- phosphofructokinase-1 is inhibited
- glycolysis is accelarated
- glycolysis is slowed down
- 1,3,6
- 2,3
- 1,4,6
- 2,5
- 2,3,5
1,4,6
2010
The oxidation of 3 moles of glucose by the pentose phosphate pathway may result in the production of
- 3 moles of pentose, 4 moles of NADPH, and 3 moles of CO2
- 2 moles of pentose, 8 moles of CO2, and 4 moles of NADPH
- 3 moles of CO2, 6 moles of NADPH, and 3 moles of pentose
- 6 moles of CO2, 6 moles of NADPH, and 4 moles of triose
- 18 moles of CO2, 18 moles of NADPH
3 moles of CO2, 6 moles of NADPH, and 3 moles of pentose
2010
Which of the following is true of the control of gluconeogenesis?
- glucagon stimulates adenylyl cyclase, causing the formation of cAMP
- Cyclic AMP stimulates the phosphorylation and thus increases the activity of FBPase-2
- FBPase-2 activity lowers the level of fructose 2,6-bisphosphate, thus increasing the rate of gluconeogenesis
- It is reciprocally linked to the control of glycolysis
- all of the above are true
all of the above are true
2010
Which of the following has the (immediate) effect of increasing the rate of glycogen breakdown?
- A- increased concentration of cAMP
- B- increase in the [AMP]/[ATP] ratio
- C- increased secretion of glucagon
- A and C
- A, B, and C
A, B, and C
2010
Which of the following correctly matches the glycolytic reaction with the gluconeogenic enzyme used in the corresponding bypass reaction?
- Glucose → glucose 6-phosphate; glucose 6-phosphatase
- Fructose 6-phosphate → fructose 1,6-bisphosphate; phosphofructokinase-2
- Fructose 1,6-bisphosphate → dihydroxyacetone phosphate + glyceraldehyde 3-phosphate; glyceraldehyde 3-phosphate dehydrogenase
- 2-Phosphoglycerate → phosphoenolpyruvate; phosphoglycerate kinase
- Phosphoenolpyruvate → pyruvate; pyruvate kinase
Glucose → glucose 6-phosphate; glucose 6-phosphatase
2010
Transport of fatty acids from the cytoplasm to the mitochondrial matrix requires:
- ATP, coenzyme A, and hexokinase
- ATP, carnitine and coenzyme A
- carnitine, coenzyme A, and hexokinase
- ATP, carnitine, and pyruvate dehydrogenase
- ATP, coenzyme A, and pyruvate dehydrogenase
ATP, carnitine and coenzyme A
2010
Lipoprotein lipase acts in
- intracellelar lipid breakdown of lipoproteins
- intestinal uptake of dietary fat
- lipoprotein breakdown to supply needed amino acids
- hydrolysis of triacylglycerols of plasma lipoproteins to supply fatty acids to various tissues
- none of the above
hydrolysis of triacylglycerols of plasma lipoproteins to supply fatty acids to various tissues
Fatty acids are activated to acyl-CoAs and the acyl group is further transferred to carnitine because
- acyl-CoAs easily cross the mitochondrial membrane, but the fatty acids themselves will not
- fatty acids cannot be oxidized by FAD unless they are in the acyl-carnitine form
- carnitine is required to oxidize NAD+ to NADH
- acyl-carnitines readily cross the mitochondrial inner membrane, but acyl-COAs do not
- None of the above is true
acyl-carnitines readily cross the mitochondrial inner membrane, but acyl-COAs do not
2010
Which of the following is (are) true of the oxidation of 1 mol of palmitate (a 16-carbon saturated fatty acid; 16:0) by the β-oxidation pathway, beginning with the free fatty acid in the cytoplasm?
- Activation of the free fatty acid requires the equivalent of two ATP
- Inorganic pyrophosphate (PPi) is produced
- Carnitine functions as an electron acceptor
- 8 mol of FADH2 are formed
- 8 mol of acetyl-CoA are formed
- there is no direct involvement of NAD+
- 1, 2, 6
- 1, 3, 5
- 1 and 5 only
- 5 only
- 1, 2, and 5
1, 2, and 5
2010
Place the following steps in lipid oxidation in their proper sequence
- a - Thiolysis
- b - Reaction of fatty acyl-ClA with carnitine
- c - Oxidation requiring NAD+
- d - Hydrolysis of triacylglycerol by lipase
- e - Activation of fatty acid by joining to CoA
- f - Hydration
- 5, 4, 3, 2, 1, 6
- 4, 5, 2, 3, 4, 1
- 4, 2, 5, 3, 6, 1
- 1, 4, 5, 2, 6, 1
- 5, 4, 2, 3, 1, 6
4, 5, 2, 3, 4, 1
d, e, b, c, f, a
- Hydrolysis of triacylglycerol by lipase
- Activation of fatty acid by joining to CoA
- Reaction of fatty acyl-ClA with carnitine
- Oxidation requiring NAD+
- Hydrolysis of triacylglycerol by lipase
- Thiolysis
2012
When the serum glucose concentrations falls below the normal level, which of the following will occur?
- A. Glycolysis in red blood cells and nerve cell slows down
- B. Glycolysis in these cells continues normally
- C. Skeletal muscle contraction stops so as to save glucose
- D. Glycolysis in liver is increased
- E. None of the above
B. Glycolysis in these cells continues normally
2012
Biological oxidation-reduction reactions always involve:
- A. direct participation of oxygen.
- B. formation of water.
- C. mitochondria.
- D. transfer of electron(s)
- E. transfer of hydrogens
D. transfer of electron(s)
2012
Which of the following statements concerning signal transduction by the insulin receptor is not correct?
- A. Activation of the receptor protein kinase activity results in the activation of additional protein kinases.
- B. Binding of insulin to the receptor activates a protein kinase.
- C. Binding of insulin to the receptor results in a change in its quaternary structure.
- D. The receptor protein kinase activity is specific for tyrosine residues on the substrate proteins.
- E. The substrates of the receptor protein kinase activity are mainly proteins that regulate transcription
E. The substrates of the receptor protein kinase activity are mainly proteins that regulate transcription
2012
Which of the following does not involve cyclic AMP?
- A. Regulation of glycogen synthesis and breakdown
- B. Regulation of glycolysis
- D. Signaling by epinephrine
- C. Signaling by acetylcholine
- E. Signaling by glucagon
C. Signaling by acetylcholine
2012
Hormone-activated phospholipase C can convert phosphatidylinositol 4,5-bisphosphate to:
- A. diacylglycerol + inositol triphosphate.
- B. diacylglycerol + inositol+ phosphate.
- C. glycerol + inositol + phosphate.
- D. glycerol + phosphoserine.
- E. phosphatidyl glycerol + inositol + phosphate.
A. diacylglycerol + inositol triphosphate.
2012
Gluconeogenesis occurs during intense exercise. This seems counter-intuitive.
- A. This is not true; two opposing pathways would result in net hydrolysis of ATP
- B. Intense exercise consumes fatty acids only,
- C. Skeletal muscle converts glucose residues to pyruvate and lactate. Rising level of lactate causes lactate to pass from muscle to blood to liver where the lactate can be converted (by gluconeogenesis) to glucose.
- D. During exercise, glucose is transported from blood into muscle. When serum glucose has been depleted, liver forms glucose by gluconeogenesis and glycogenolysis.
- E. Insulin activates the Glut 4 and glucose transport into muscle increases.
C. Skeletal muscle converts glucose residues to pyruvate and lactate. Rising level of lactate causes lactate to pass from muscle to blood to liver where the lactate can be converted (by gluconeogenesis) to glucose.
2012
In the coordinated control of glycolysis and gluconeogenesis in liver
- A. Citrate inhibits PFK and stimulates F-1 ,6-Bpase.
- B. Fructose 2,6-bisphosphate stimulates F-1,6-Bpase and inhibits PFK.
- C. Acetyl CoA inhibits PFK and stimulates F-1,6-Bpase.
- D. AMP inhibits PFK and stimulates F-1,6-Bpase.
- E. NADPH inhibits PFK and stimulates F-1,6-Bpase.
A. Citrate inhibits PFK and stimulates F-1 ,6-Bpase.
Avidin, a 70-kd protein in egg white has a high affinity for biotin. In fact, it is a highly specific inhibitor of biotin enzymes. Which of the following conversions would be blocked by the addition of avidin to a cell homogenate?
- A. Glucose → Pyruvate
- B. Pyruvate → Glucose
- C. Oxaloacetate → Glucose
- D. Malate →oxaloacetate
- E. Glyceraldehyde-3-P → Fructo 1 ,6-Bis P
B. Pyruvate → Glucose
2012
Glucose, labeled with 14C in different carbon atoms, is added to a crude extract of a tissue rich in the enzymes of the pentose phosphate pathway. The most rapid production of 14CO2 will occur when the glucose is labeled in:
- A. C-1
- B. C-3
- C. C-4
- D. C-5
- E. C-6
A. C-1
2012
Glucose labeled with 14C at C-6 is added to a solution containing the enzymes and cofactors of the oxidative branch of the pentose phosphate pathway. The radioactive label will be found in D-ribulose-5P at
- A. C-1
- B. C-2
- C. C-3
- D. C-4
- E. C-5
E. C-5
2012
When blood glucagon rises, which of the following hepatic enzyme activities FALLS?
- A. adenyl cyclase
- B. protein kinase A
- C. 6-phosphofructo-2-kinase
- D. fructose 1 ,6-bisphosphatase
- E. hexokinase
E. hexokinase
2012
Malignant hyperthermia is a genetic abnormality in which exposure to certain agents, especially the widely used general anesthetic halothane, produces a dramatic rise in body temperature, acidosis, hyperkalemia, and muscle rigidity. Death is rapid if the condition is untreated and may occur the first time a susceptible person is anesthetized. The defect causes an inappropriate release of Ca2+ from the sarcoplasmic reticulum of muscle. Many heat producing processes are stimulated in an uncontrolled fashion by the release of Ca2+, including glycolysis and glycogenolysis.
Ca2+ increases glycogenolysis by:
- A. activating phosphorylase kinase b, even in the absence of cAMP
- B. binding to phosphorylase b.
- C. activating phosphoprotein phosphatase.
- D. inhibiting phosphoprotein phosphatase. E. protecting cAMP from degradation.
A. activating phosphorylase kinase b, even in the absence of cAMP
2012
Malignant hyperthermia is a genetic abnormality in which exposure to certain agents, especially the widely used general anesthetic halothane, produces a dramatic rise in body temperature, acidosis, hyperkalemia, and muscle rigidity. Death is rapid if the condition is untreated and may occur the first time a susceptible person is anesthetized. The defect causes an inappropriate release of Ca2+ from the sarcoplasmic reticulum of muscle. Many heat producing processes are stimulated in an uncontrolled fashion by the release of Ca2+, including glycolysis and glycogenolysis.
Phosphorylation-dephosphorylation and allosteric activation of enzymes play roles in stimulating glycogen degradation. All of the following result in enzyme activation EXCEPT:
- A. phosphorylation of phosphorylase kinase.
- B. binding of AMP to phosphorylase b.
- C. phosphorylation of phosphorylase
- D. phosphorylation of protein kinase A.
- E. dephosphorylation of glycogen synthase.
D. phosphorylation of protein kinase A.
2012
Malignant hyperthermia is a genetic abnormality in which exposure to certain agents, especially the widely used general anesthetic halothane, produces a dramatic rise in body temperature, acidosis, hyperkalemia, and muscle rigidity. Death is rapid if the condition is untreated and may occur the first time a susceptible person is anesthetized. The defect causes an inappropriate release of Ca2+ from the sarcoplasmic reticulum of muscle. Many heat producing processes are stimulated in an uncontrolled fashion by the release of Ca2+, including glycolysis and glycogenolysis.
Which one of the following is not a characteristic of phosphoprotein phosphorylase-1 (PP1)?
- A. PP1 can be phosphorylated by protein kinase A (PKA).
- B. PP1 can dephosphorylate glycogen phosphorylase, glycogen synthase, and phosphorylase kinase.
- C. PP1 is allosterically activated by glucose-6-phosphate.
- D. PP1 is inhibited by activated glycogen phosphorylase
- E. PP1 is phosphorylated by glycogen synthase kinase-3 (GSK3).
E. PP1 is phosphorylated by glycogen synthase kinase-3 (GSK3).
2012
The role of hormone-sensitive triacylglycerol lipase is to:
- A. hydrolyze lipids stored in the liver.
- B. hydrolyze membrane phospholipids in hormone-producing cells.
- C. hydrolyze triacylglycerols stored in adipose tissue.
- D. synthesize lipids in adipose tissue.
- E. synthesize triacylglycerols in the liver.
C. hydrolyze triacylglycerols stored in adipose tissue.
2012
Which of the following statements concerning the β oxidation of fatty acids is true?
- A. About 1,200 ATP molecules are ultimately produced per 20-carbon fatty acid oxidized.
- B. One FADH2 and two NADH are produced for each acetyl-CoA.
- C. The free fatty acid must be carboxylated in the β position by a biotin-dependent reaction before the process of β oxidation commences.
- D. The free fatty acid must be converted to a thioester before the process of β oxidation commences.
- E. Two NADH are produced for each acetyl-CoA.
D. The free fatty acid must be converted to a thioester before the process of β oxidation commences.
2012
The balanced equation for the degradation of CH3(CH2)10COOH via the β-oxidation pathway is:
- A. CH3(CH2)10COOH + 5FAD + 5NAD+ + 6CoA—SH + 5H2O + ATP → 6 Acetyl-CoA + 5FADH2 + 5NADH + 5H+ + AMP + PPi
- B. CH3(CH2)10COOH + 5FAD + 5NAD+ + 6CoA—SH + 5H2O → 6 Acetyl-CoA + 5FADH2 + 5NADH + 5H+
- C. CH3(CH2)10COOH + 6FAD + 6NAD+ + 6CoA—SH + 6H2O + ATP → 6 Acetyl-CoA + 6FADH2 + 6NADH + 6H+ + AMP + PPi
- D. CH3(CH2)10COOH + 6FAD + 6NAD+ + 6CoA—SH + 6H2O → 6 Acetyl-CoA + 6FADH2 + 6NADH + 6H+
A. CH3(CH2)10COOH + 5FAD + 5NAD+ + 6CoA—SH + 5H2O + ATP → 6 Acetyl-CoA + 5FADH2 + 5NADH + 5H+ + AMP + PPi
2013
Restriction enzymes
- A. used in Northern analysis
- B. used for protein processing
- C. recognize palindromic sequences of DNA
- D. recognize palindromic sequences of RNA
- E. cut randomly in the genome
C. recognize palindromic sequences of DNA
2013
PCR:
- A. stands for polymer chain response
- B. can only use DNA as a template
- C. can be used to amplify RNA sequences
- D. requires gel electrophoresis for detection
- E. is used in western analysis
B. can only use DNA as a template
2013
mRNA:
- A. is the most abundant RNA in the cell
- B. can be separated from other RNA species by polyA isolation
- C. can be analyzed by Southern analysis
- D. is not really important
- E. can be used as a template for PCR
B. can be separated from other RNA species by polyA isolation
2013
Generation of a knockout animal involves:
- A. homologous recombination
- B. random insertion of exogenous DNA
- C. targeted insertion of exogenous RNA
- D. use of siRNA to eliminate DNA expression
- E. competent rat species
A. homologous recombination
2013
Which of the following is a true statement about DNA:
- A. All DNA in a eukaryotic organism is in heterochromatin form unless activated
- B. Prokaryotic DNA is capped by telomere sequences
- C. 1.5% of eukaryotic DNA is considered genes
- D. All DNA in eukaryotic organisms is in euchromatin form unless activated
- E. 1.5% of all eukaryotic DNA is coding.
E. 1.5% of all eukaryotic DNA is coding.
2013
fMet :
- A. is the last amino acid added to the polypeptide chain
- B. is necessary for the elongation step of translation
- C. only exists in the tRNA structure
- D. has a specific tRNA separate from Met.
- E. has a different codon than Met
D. has a specific tRNA separate from Met
2013
Eukaryotic translation:
- A. is exactly the same as prokaryotic transcription
- B. requires a multiprotein complex that links the transcribed RNA to the translational machinery via the 5’ cap and poly A tail.
- C. does not use AUG as the start codon
- D. requires a shine-delgardo sequence to start translation.
- E. is dependant on the sigma factor
B. requires a multiprotein complex that links the transcribed RNA to the translational machinery via the 5’ cap and poly A tail.
2013
RNA polymerase II is distinct in that it
- A. Is only used to generate tRNAs
- B. Is only found in eukaryotic organisms
- C. Is effective on a variety of different promoters
- D. Is used to make primers for DNA replication
- E. Makes Okazaki fragments.
C. Is effective on a variety of different promoters
2013
In prokaryotes, RNA polymerase finds the start of transcription by:
- A. Specific sequences in the promoter region
- B. Identification of the cap structure
- C. Sliding along the DNA and looking for unwound segments
- D. Signaling the histone molecules to disconnect from the wound DNA
- E. Sliding along the DNA to find a specific stem-loop structure
A. Specific sequences in the promoter region