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20 Cards in this Set
- Front
- Back
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The _____ provides Ribose-5-phosphate used for purine synthesis. What are the next 8 steps (AGGFGCAF)? What compound do you end up with?
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- PP shunt
1) add ATP --> AMP (2 phosphates) to make PRPP 2) PRPP --> 5 phosphoribosyl-1-amine (by adding amino via glutamine --> glutamate) 3) add glycine --> ribose-P 4) add N10 folate 5) add amino via Gln --> Glu 6) add CO2 7) add aspartate 8) add N10 folate - end up with IMP |
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IMP + ________ --> adenylosuccinate --> ______. This requires GTP. IMP --> ______ --> ______. This requires ATP.
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- aspartate
- AMP - Xanthylate - GMP |
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The conversion of monophosphates to diphosphates is catalyzed by kinases that are____-specific but not ____-specific
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- base
- sugar - ex. GMP kinase |
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________ converts diphosphates to triphosphates. This enzyme has broad specificity.
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- nucleoside diphosphate kinase
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In order for AZT to work it must be converted to _______. This is done by the action of ______, ______ & then ______.
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- AZT triphosphate
- thymine kinase - thymidylate kinase - nucleotide diphosphate kinase |
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The purine ring contains which 5 compounds?
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1) Gluamine
2) Glycine 3) Folate 4) CO2 5) Aspartate |
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Biosynthesis of purines requires ___ ATP driven reactions. The glycosidic bond is formed when the first atom of the purine ring is incorporated. This is the committed step & is catalyzed by __________.
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- 4
- PRPP amidotransferase |
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The first purine synthesized is _____, the precursor for AMP & GMP. De novo synthesis is particularly active in the ____ & ____.
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- IMP
- liver & placenta |
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_____ works on guanine & hypoxanthine to add them to PRPP and form what? _____ works on adenine to add it to PRPP to form what?
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- HGPRT
- guanine + PRPP = GMP - hypoxanthine + PRPP = IMP - APRT - adenine + PRPP = AMP |
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In the first step of purine (adenine) catabolism, monophosphates are converted to nucleosides by _______. Then they are ______. Then a ______ acts on them to break the glycosydic bond and leaves the product ________. What is different about the breakdown of guanine?
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- phosphatases
- deaminated - phosphorylases - ribose-1-phosphate - guanine isn't deaminated until after the phosphorylase breaks the glycosydic bond |
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hypoxanthine via ______ is broken down to ______ which can further be acted on by _______ to give you ______. Guanine via _____ is broken down to ______ which can further be acted on by _______ to give you ______.
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- xanthine oxidase
- xanthine - xanthine oxidase - uric acid - guanine deaminase - xanthine - xanthine oxidase - uric acid |
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amidotransferase is an enzyme of the _____ pathway, whereas phosphoribosyltransferase is an enzyme of the ____
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- de novo
- salvage |
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As you build up ATP & GTP they negatively feed back on ____________ & ___________. When you build up PRPP what does it do?
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- PRPP synthetase
- phosphoribosyltransferase - activates synthesis of purine nucleotides |
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Gout is characterized by elevated ______ levels in the blood, due to a variety of metabolic abnormalities.
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- uric acid
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What 3 enzyme defects can lead to gout and why?
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1) defective HGPRT: reduced IMP & GMP formation via salvage pathway - PRPP accumulates & causes activation of de novo pathway & reduced neg. feedback
2) PRPP synthetase less susceptible to feedback inhibition by purine nucleotides - overproduction of PRPP & activation of de novo pathway 3) glucose-6-phosphatase deficiency: leads to increased utilization of PP shunt & consequently excessive production of ribose-5-phosphate (immediate precursor of PRPP) |
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Allopurinol is an analog of ________. What does it do?
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- hypoxanthine
- competitive inhibitor of xanthine oxidase (which converts xanthine --> uric acid) - upon treatment hypoxanthine & xanthine accumulate - which are more soluble and more easily secreted |
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Lesch-Nyhan syndrome
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- lack HGPRT
- self-mutilation, gout like symptoms, increase in de novo pathway - usually HGPRT activity is high in brain - suggests important of purine salvage in this tissue |
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With ADA deficiency you end up with ______ like symptoms
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- SCID
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Sulfoamides resemble ______ & inhibit ____ synthesis in bacteria.
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- p-aminobenzoic acid
- folate - since no folic acid - no synthesis of purines & they die |
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_______ is an inhibitor of purine biosynthesis used in the treatment of acute leukemia. Functions as an analogue of hypoxanthine. How does it work?
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- 6-mercaptopurine
- once you add it to PRPP it is a competitive inhibitor of IMP which gives rise to AMP & GMP |
