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Nucleotides
UCI SOM Moyzis
| Question | Answer |
|---|---|
| Bases | adenine, guanine, cytosine, uracil, thymine |
| Nucleosides | adenosine, guanosine, cytidine, uridine, thymidine |
| PRPP | activates first step of purine synthesis (the commited step); PRPP synthesis is inhibited by purines |
| Glutamine:phosphoribosyl pyrophosphate amidotransferase | first and commited step of purine synthesis |
| Inosine monophosphate | parent purine nucleotide |
| Are purines formed on their ribose | yes |
| Are pyrimidines formed on their ribose | no |
| Sulfonamides | inhibit bacterial purine synthesis by inhibiting folic acid synthesis, blocking THF formation |
| Methotraxate | inhibit dihydrofolate reduction to THF, blocking purine synthesis in humanstrimethoprim |
| Mycophenolic acid | reversible inhibitor of GMP synthesis; used to prevent graft rejection |
| What two amino acids are used in both purine and pyrimidine synthesis | glutamine and aspartic acid |
| Carbamoyl phosphate | first product in pyrimidine synthesis; it’s production is the regulated step |
| CPS II | carbamoyl phosphate synthetase |
| Orotic acid | intermediate product in pyrimidine synthesis |
| The enzyme that produces orotic acid is found where in the cell | mitochondrial membrane (all other enzymes are cytosolic) |
| What’s special about the first three enzymes in pyrimidine synthesis | different domains on same protein |
| Orotic aciduria | last two enzymes are different domains of single protein and when this protein is deficient, orotate accumulates |
| Ribonucleotide reductase | makes DNA’s from RNA’s |
| When in the cell cycle does ribonucleotide reductase function | S-phase |
| Regulation of ribonucleotide reductase | each dNTP regulates its own synthesis; dATP inhibits all of them |
| 5-fluorouracil | suicide enzyme; inhibits dUMP to dTMP synthase |
| thymidylate synthase | enzyme that converts dUMP to dTMP |
| methotrexate | inhibits the reduction of DHF to THF in dUMP to dTMP conversion |
| where does degredation of dietary nucleic acids occur | small intestine |
| what happens to most dietary purines | converted to uric acid |
| what happens to most dietary pyrimidines | degraded to highly soluble products |
| diseases associated with purine degredation | gout, adenosine deaminase (ADA) deficiency |
| gout | hyperuricemia, doposition of monosodium urate crystals in joints; gouty arthritis; idiopathic; increased risk with lots of meat, seafood, legumes |
| treatment of gout | anti-inflammatory drugs; allopurinol inhibits urate |
| ADA deficiency | accumulation of adenosine |
| HGPRT | enzyme in purine salvage pathway that is deficient in lesch-nyhan syndrome; uses PRPP |
| Lesch nyhan syndrome | extreme gout; lack of HGPRT enzyme; self mutilation |
| Neurotransmitters | domapine, norepinephrine, epinephrine, serotonin |
| Epinephrine synthesis pathway | phenylalanine, tyrosine, dopa, dopamine, norepi, epi |
| MAO | inactivates catecholamines by degredation along with COMT |
| COMT | inactivates catecholamines by degredation along with MAO |
| MAO inhibitor | permits neurotransmitter molecules to escape degredation (used for antidepression) |
| Methylphenidate | ritalin; blocks dopamine re-uptake; used to treat ADHD |
| Cocaine | similar actions to methylphenidate |
| Prozac and paxil work by | blocking serotonin transporter |
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