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1
Q

What is the general name of the enzymes that catalyse the transamination reactions?

A

Transaminase or amino trasnferase

2
Q

Why are transamination reactions important?

A
  • Involved in both synthesis and catabolism of amino acids
  • Route for the redistribution of amino acid nitrogen
  • First step in catabolism of most amino acids once they have reached the liver
3
Q

What is the relationship between the reaction catalysed by glutamate dehydrogenase and the urea cycle?

A

Glutamate dehydrogenase releases the amino group from glutamate. The free NH4+ can then enter the urea cycle

4
Q

In which tissue does the urea cycle occur?

A

Liver

5
Q

Why is the function of the urea cycle important?

A

The urea cycle converts toxic not very water soluble ammonium ions to less toxic and more water soluble urea which can be readily removed from the body

6
Q

What are the enzymes that catalyse the three irreversible steps in glycolysis?

A

Heoxkinase
Phosphofructokinase-1
Pyruvate kinase

7
Q

What is the substrate and product of hexokinase?

A

Glucose -> Glucose-6-phosphate

8
Q

What regulates hexokinase? Does it inhibit or stimulate?

A

Glucose (stimulates)

9
Q

What is the substrate and product of phosphofructokinase-1?

A

Fructose-6-phosphate -> Fructose 1,6, bisphosphate

10
Q

What regulates phosphofructokinase-1? Does it inhibit or stimulate?

A
Fructose-6-P (stimulates)
ATP (inhibits)
AMP (stimulates)
ADP (stimulates)
Citrate (inhibits)
11
Q

What is the substrate and product of pyruvate kinase?

A

Phophoenol pyruvate -> pyruvate

12
Q

What regulates pyruvate kinase? Does it inhibit or stimulate?

A

ATP (inhibits)
Acetyl CoA (inhibit)
Glucagon (inhibit)

13
Q

True or False:

Glycogen synthase is active in the dephosphorylated form

A

True

14
Q

True or False:

Insulin results in the phosphorylation of glycogen synthase

A

False

15
Q

True or False:

Glycogen synthase kinase is responsible for the activation of glycogen synthase

A

False

16
Q

True or False:

Glucose-6-phosphate is an allosteric activator of glycogen synthase

A

True

17
Q

Describe the impact of a deficiency of the enzyme adenosine deaminase including the molecular changes that occur

A

loss of ADA activity results in:
• increased dATP levels (1 mark)
• dATP is a feed back inhibitor of ribonucleotide reductase therefore high dATP reduces synthesis of other dNTP’s (1 mark)
• reduced dNTP pool effects T and B cell proliferation (1 mark)

(0.5 each – max of 1 1 mark )
• susceptibility to infectious diseases
• total inability to mount an immune response
• T and B lymphocytes are affected

18
Q

b. What is the general name of the enzymes that catalyse the transamination reactions?

A

Transaminase or amino transferase (either accepted)

19
Q

c. Why are transamination reactions important?

A
  • involved in both synthesis & catabolism of amino acids
  • Route for the redistribution of amino acid nitrogen
  • 1st step in catabolism of most amino acids once they have reached the liver
20
Q

d. What is the relationship between the reaction catalysed by glutamate dehydrogenase and the urea cycle?

A

Glutamate dehydrogenase releases the amino group from glutamate. The free NH4+ can then enter the urea cycle

21
Q

e. In which tissue does the urea cycle occur?

A

Liver

22
Q

f. Why is the function of the urea cycle important?

A

The urea cycle converts toxic not very water soluble ammonium ions to less toxic and more water soluble urea which can be readily removed from the body

23
Q

Explain the differences in carbohydrate metabolism between a person with normal metabolism and a person with untreated Type 1 Diabetes immediately after a meal.

A
  • Instead of glucose being taken up by the liver after a meal and either used in glycolysis or stored as glycogen ….
  • Glucose is released from the liver (from either glycogen stores or synthesised by gluconeogenesis) into the blood stream.
24
Q

Explain the differences in lipid metabolism between a person with normal metabolism and a person with untreated Type 1 Diabetes immediately after a meal.

A
  • Instead of fatty acids being taken up by adipocytes and stored as triacylglycerols after a meal..
  • stored triacyl glycerols are broken down to fatty acids and glycerol both of which are released into the blood stream.
25
Q

Which hormone class does aldosterone belong to?

A

Steroid

26
Q

Which hormone class does Growth hormone belong to?

A

Peptide

27
Q

Which hormone class does thyroid hormones belong to?

A

Amine

28
Q

Which hormone class does testosterone belong to?

A

Steroid

29
Q

Which hormone class does cortisol belong to?

A

Steroid

30
Q

Which hormone class does insulin belong to?

A

Peptide

31
Q

Receptor tyrosine kinases have a characteristic sequence of events upon activation. What TWO major events occur after the binding of a ligand to a monomeric target receptor tyrosine kinase?

A

Receptor dimerisation

Autophosphorylation

32
Q

Transcription factors are _____-binding proteins. For example, a Hox protein has a conserved 60 amino acid domain called the __________.

A

DNA; homeodomain

33
Q

A ___________ transformation occurs when one body part develops as a different body part, such as legs instead of antennae in the fly.

A

Homeotic

34
Q

In mammals, there are four sets of Hox genes, derived by ancestral duplication. Related genes in the series (Hoxa13, Hoxb13, Hoxc13 and Hoxd13, for example) are called _________.

A

Paralogues

35
Q

Describe three types of genetic modifications that convert a proto-oncogene into an oncogene

A

1
An activating mutation in a DNA coding sequence (deletion or point mutation) – hyperactive protein made in normal amounts

Gene Amplification – normal protein greatly overproduced

Chromosomal translocation – hyperactive fusion protein produced or nearby regulatory sequence causes normal protein to be greatly overproduced

36
Q

What is an example of a proto-oncogene that is converted into an oncogene by point mutation?

A

Ras

37
Q

What is an example of a proto-oncogene that is converted into an oncogene by gene amplification?

A

EGFR2 (HER2)
or
MYC

38
Q

What is an example of a proto-oncogene that is converted into an oncogene by chromosomal translocation?

A

BCR-ABL