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DMD 5243 > Nucleotide Metabolism (complete) > Flashcards

Nucleotide Metabolism (complete) Flashcards

1
Q

Which bases are purines

A

Adening

Guanosine

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2
Q

which bases are pyrimidines

A

Cytosine
thymine
Uracil

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3
Q

what is the structure of the pyrimidines

A

an individual 6 membered ring

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4
Q

what is the structure of purines

A

a 2 membered ring with an attached 5 membered ring

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5
Q

how do you differentiate between Adenine and Guanosine

A

Adenine has a NH2

Guanine has a carbonyl

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6
Q

how do you differentiate between Cytosine, thymine, and uracil

A

Cytosine has NH2
thymine has a methyl group
Uracil has neither

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7
Q
  1. Nucleotides are only involved in RNA and DNA synthesis
    a. True
    b. False
A

False

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8
Q
  1. A nucleoside is
    a. A nucleobase
    b. A nucleobase and a ribose sugar
    c. A nucleobase, a ribose sugar and a phosphate group
    d. A nucleobase, a ribose sugar, a phosphate group and acetyl CoA
A

B

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9
Q
  1. Purine biosynthesis regulated by:
    a. AMP,
    b. ADP
    c. IMP
    d. GMP
    e. All of the above
A

E

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10
Q
  1. Which is the final step in the pathway for pyrimidine biosynthesis
    a. UMP
    b. CMP
    c. TMP
    d. TTP
A

B

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11
Q
  1. 5-fluorouracil is an inhibitor of
    a. purine bio synthesis
    b. pyrimidine biosynthesis
    c. thymidine synthesis
    d. Adenosine synthesis
A

C

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12
Q
  1. Another name for an anti-metabolite is:
    a. Anti-toxin
    b. Anti-freeze
    c. Inhibitor
    d. Allosteric modifier
A

Inhibitor

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13
Q
  1. Ribonucleotide Reductase activates the tyrosine radical with
    a. Iron cofactor
    b. Copper cofactor
    c. NAD cofactor
    d. Folate cofactor
A

A

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14
Q

What are the functions of nucleotides

A 
Energy for metabolism (ATP)
Enzyme cofactors (NAD+)
Signal transduction (cAMP)
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15
Q

what are the functions of nucelic acids

A

Storage of genetic info (DNA)
transmission of genetic info (mRNA)
processing genetic info (ribozymes)
protein synthesis (tRNA and rRNA)

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16
Q

What is a nucleobase

A

nitrogenous base (A, T, U, C, G)

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17
Q

What is a nucleoside

A

nitrogenous base and a pentose (the sugar)

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18
Q

What is a nucleotide

A

nitrogenous base, pentose, and phosphate (1, 2, or 3)

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19
Q

in de novo biosynthesis of purines are the bases and ribose made seperately and then put together

A

no, the base is synthesized while attached to the pentose

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20
Q

what is the pentose used in DNA and RNA

A

ribose

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21
Q

what amino acid provides most amino groups for newly made nucleotides

A

Gln (glutamine)

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22
Q

what is the precursor for purines

A

glycine (gly)

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23
Q

what is the precursor for pyrimidines

A

Asp (aspartic acid)

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24
Q

What things contribute to the formation of a purine

A 
aspartate (N)
CO2 (C)
formate (2-Cs)
glycine (C=C-N)
glutamine (2-Ns)

ACFGG

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25
Q

what does de novo biosynthesis of purines begin with

A

PRPP

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26
Q

in the de novo biosynthesis of purines what does PRPP interact with

A

Gln (adds an N)

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27
Q

after PRPP has reacted with Gln in de novo biosynthesis what does that molecule interact with

A

Gly (adds C=C–N)

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28
Q

What is the first intermediate in de novo biosynthesis of purines that has a full purine ring

A

inosinate (IMP)

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29
Q

what things can by synthesized from IMP

A

Adenine and Guanine

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30
Q

How does inosinate (IMP) get converted to Adenylate (AMP)

A
  1. inosinate + aspartate and GTP = adenylsuccinate

2. Adenylsuccinate + Fumerate = adenylate

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31
Q

how does inosinate (IMP) get converted to Guanylate (GMP)

A
  1. inosinate + H2O and NAD+ = xanthylate (XMP)

2. XMP + Gln and ATP = Guanylate

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32
Q

What are the enzymes required to turn IMP into AMP

A
  1. adenylosuccinate synthetase

2. adenylosuccinate lyase

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33
Q

what are the enzymes required to turn IMP into GMP

A
  1. IMP dehydrogenase

2. XMP glutamine amidotransferase

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34
Q

What are the five major mechanisms of regulation of purine biosynthesis

A
  1. glutamine-PRPP amidotransferase is inhibited by IMP, AMP, GMP
  2. IMP dehydrogenase inhibited by GMP
  3. Adenylosuccinate synthetase inhibited by AMP
  4. GTP limits conversion of IMP to AMP, ATP limits conversion of IMP to GMP
  5. PRPP synthesis is inhibited by ADP and ADP
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35
Q

What inhibits the first enzyme in de novo biosynthesis of purines

A

IMP, AMP, GMP

the products of de novo biosynthesis of purines

36
Q

What is the first enzyme in de novo biosynthesis of purines

A

glutamine- PRPP amidotransferase

37
Q

What inhibits the enzyme IMP dehydrogenase, and that prevents the synthesis of what

A

GMP inhibits IMP dehydrogenase

that prevents the formation of XMP (and thus GMP)

38
Q

what inhibits the enzyme adenylosuccinate synthetase, and that prevents the synthesis of what

A

AMP inhibits adenylosuccinate

that prevents the formation of adenylosuccinate ( and thus AMP)

39
Q

What effect does GTP have on de novo biosynthesis

A

it limits the conversion of IMP to AMP

40
Q

what effect does ATP have on de novo biosynthesis

A

it limits the conversion of IMP to GTP

41
Q

What inhibits the formation of PRPP

A

ADP and GDP

42
Q

what is a main way that purine and pyrimidine biosynthesis differ

A

in purine biosynthesis the purine ring is made onto the ribose
in pyrimidine biosynthesis the pyrimidine ring is made, then attached to the ribose

43
Q

what is the first step in biosynthesis of pyrimidines

A

Asp and N-carbamoylphosphate

44
Q

what is the enzyme that catalyzes the Asp and N-carbamoylphosphate reaction that begins de novo biosynthesis of pyrimidines

A

ATCase (aspartate transcarbamoylase)

45
Q

what is the main intermediate of pyrimidine synthesis, the one that is made first, and from there you make all of the others

46
Q

how do you get from UMP to CTP

A

UMP is converted to UTP, then UTP is converted to CTP

47
Q

does TMP come from UMP or CTP

48
Q

how do you get TMP from UMP

A

UMP –> UDP –> dUDP –> dUTP –> dUMP –>dTMP

49
Q

how do you get TMP from CTP

A

CTP –> CDP –> dCDP –> dCTP –> dUTP –> dUMP –> dTMP

50
Q

How is de novo pyrimidine synthesis regulated

A

CTP (the end product) inhibits aspartate trans carbamoylase (the first enzyme)
ATP accelerates aspartate carbamoylase

51
Q

what inhibits de novo pyrimidine synthesis

52
Q

what accelerates de novo pyrimidine synthesis

53
Q

what is the enzyme that helps convert dUMP to dTMP

A

thymidylate synthase

54
Q

what does the conversion of dUMP to dTMP by thymidylate synthase create (though indirectly)

A

tetrahydrofolate (THF)

55
Q

in dUMP and dTMP and all of those things with the d, what does the d stand for

A

Deoxygenized versions of those molecules

56
Q

What happens to levels of TMP when you have low levels of folic acid

A

with low levels of folic acid you can’t turn UMP into TMP

57
Q

what happens to the DNA when you have low levels of folic acid, and thus low levels of TMP

A

UMP can’t be converted to TMP so Uracil gets put into the DNA instead of thymine

58
Q

What happens to DNA with uracil in it (this happens with a lack of folic acid, and thus low levels of TMP)

A

repair mechanisms remove the uracil by creating strand breaks that affect the structure and function of DNA (this is associated with cancer, heart disease, and neurological impairment)

59
Q

Why is THF a good target for cancer treatment

A

because if you inhibit the thymidylate synthase in targeted cancer (causing its DNA to be altered)

60
Q

what is another name for an antimetabolite

A

an inhibitor

61
Q

what are antifolates

A

drugs that block the action of folate

62
Q

what are the two main antifolates important to dTMP production

A

fluorouracil

methotrexate

63
Q

What does the anti-folate drug fluorouracil do

A

it is converted into FdUMP which inhibits thymidylate synthase

64
Q

what does the anti-folate drug methotrexate do

A

inhibits dihydrofolate reductase, this is what makes THF (competitive inhibitor)

65
Q

what is the difference between competitive inhibitors and suicide inhibitors

A

competitive inhibitors bind to enzymes temporarily and block it from binding to its usually substrate, they come off and the enzyme is ready to bind to its substrate
suicide inhibitors bind to enzymes permanently, so that it will never bind to its substrate again

66
Q

What does ribonucleotide reductase do

A

it initiates radical chemistry and takes the 2’ OH group and puts a 2’ H group

67
Q

are there multiple pathways that activate ribonucleotide reductase

68
Q

why are there multiple ways to activate ribonucleotide reductase

A

because it is such an important enzyme that if one pathway shuts down there has to be another way to activate it or we will suffer serious consequences

69
Q

what is the structure of ribonucleotide reductase

A

it is a tetramer

70
Q

What are the substrates of ribonucleotide reductase

A

ADP
UDP
CDP
GDP

71
Q

What are the products of ribonucleotide reductase

A

dATP
dUDP
dCDP
dGDP

72
Q

What things regulate ribonucleotide reductase

A

ATP (activates it)
dATP (deacitvates it)

low amounts of a certain NTP can make the ribonucleotide reductase synthesize more of that certain NTP

73
Q

what happens in the salvage pathway

A

free bases react with PRPP to reform nucleotides

74
Q

When purines are degraded what is the end product

75
Q

how does AMP get converted into Uric acid

A

AMP –> IMP –> hypoxanthine –> xanthine –> uric acid

76
Q

how does GMP get converted into uric acid

A

GMP –> Guanine –> xanthine –> uric acid

77
Q

When pyrimidines are degraded what are the end products

A

Succinyl-CoA (used in Citrate cycle)

NH4 (then to urea)

78
Q

What causes Lesch-Nyhan syndrome

A

overproduction of uric acid

79
Q

who is mostly affected by Lesch-Nyhan syndrome

80
Q

what are the characteristics of Lesch-Nyan syndrome

A

neurological and behavioral abnormalities
gouty arthritis
uric acid accumulation in the kidney and bladder
involuntary muscle movements
people can’t walk
self injury is most common and distinctive

81
Q

what is orotic aciduria

A

the excessive secretion of orotic acid in the urine

82
Q

what does orotic aciduria cause

A

a form of anemia and mental and physical retardation

83
Q

what type of anemia is associated with orotic aciduria

A

megaloblastic anemia

84
Q

the disturbance of what pathway leads to orotic acidura

A

the pyrimidine synthesis pathway

85
Q

how is orotic aciduria treated

A

by administering CMP and UMP

DMD 5243 (17 decks)

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