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34 Cards in this Set
- Front
- Back
- 3rd side (hint)
What is heterochromatin |
Condensed chromatin, appears dark in EM |
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What is euchromatin |
Less condensed chromatin, appears lighter in EM |
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Why is important dna methylation? |
Adenine and cytosine methylation in dna replication, allows mismatch repair enzymes to distinguish between old and new strands Dna methylation at CpG represses transcription |
CpG methylation makes dna mute |
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What does histone methylation? |
It Usually represses transcription but can activate in some cases |
Histone methylation mostly make dna mute |
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What does histone acetylation |
Relaxes dna coiling, allowing transcription |
Histone acetylation makes dna active |
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Amino acids necessary for purine synthesis |
Glycine, aspartate, glutamine |
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Why are histones positively charged |
A lot of lysine and arginine, dna is negatively charged due to phosphate groups |
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Rate limiting enzyme for pyrimidine synthesis |
Carbamoyl phosphate snythtase II, requires atp, CO2 and nitrogen source is glutamine, cps II is found in cytosol |
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Which are the nucleotide synthesis interfering drugs |
-Leflunomide inhibits dihydroorotate dehydrogenase -hydroxyurea inhibits ribonucleotide reductase -5Flourouracil inhibits thymidylate synthase (⬇dTMP) -Methotrexate, trimethoprim amd pyrimethamine inhibit dihydrofolate reductase in humans, bacteria and protozoa respectively (⬇dTMP) -Mycophenolate inhibits IMP dehydrogenase - 6 mercaptopurine and prodrug azathioprine inhibit de novo synthesis of purines |
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how does adenosine deaminase compromised deficiency? |
Adenosine deaminase increase ATP and dATP leading to inhibition of ribonucleotide reductase ->prevents DNA synthesis and decrease lymphocytes Adenosine is toxic to lymphocytes decreasing humoral and cellular immunity |
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What is Lesch-nyhan syndrome? |
X-Linked, absence of HGPRT, which converts hypoxanthine in IMP, guanosine in GMP, causing hyperuricemia, gout, self mutilation, intellectual disability and dystonia |
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Origin of replication |
base pair in genome where DNA replication begins, single in procaryotes and multiple in eukaryotes |
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Replication fork
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Y-shaped region along DNA template whereleading and lagging strands are synthesized
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Helicase
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Unwinds DNA template at replication fork
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Single-strandedbinding proteins
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Prevent strands from reannealing
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DNAtopoisomerases
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Create a single- or double-stranded break in thehelix to add or remove supercoils.
flouroquinolones topoisomerase II and IV Etoposide/teniposide eukaryotic topoisomerase |
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Primase
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Makes an RNA primer on which DNApolymerase III can initiate replication
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DNA Polymerase III
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DNA polymerase III has 5′ 3′ synthesis andproofreads with 3′ 5′ exonuclease.
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DNA polymerase I
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Degrades RNA primer;replaces it with DNA
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DNA ligase
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Catalyzes the formation of a phosphodiesterbond within a strand of double-stranded DNA
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Telomerase
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An RNA-dependent DNA polymerase that addsDNA to 3′ ends of chromosomes to avoid lossof genetic material with every duplication
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what is a transition |
purine to purine substitution or pyrimidine to pyrimidine |
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what is a transversion |
purine to pyrimidine substitution or pyrimidine to purine |
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severity of substitutions in DNA mutation |
severity of damage silent< |
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What is a silent substitution |
Nucleotide substitution but codes for same(synonymous) amino acid; often base changein 3rd position of codon
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What is a missense substitution |
Nucleotide substitution resulting in changedamino acid.
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sickle cell disease |
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What is a nonsense substitution |
Nucleotide substitution resulting in early stopcodon. Usually results in nonfunctionalprotein.
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What is a frameshift mutation |
Deletion or insertion of a number of nucleotidesnot divisible by 3, resulting in misreading ofall nucleotides downstream. Protein may beshorter or longer, and its function may bedisrupted or altered
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What is a splice site mutation |
Mutation at a splice site-> retained intron inthe mRNA ->protein with impaired or alteredfunction
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Nucleotide excisionrepair
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Repairs bulky helix-distortinglesions. Occurs in G1. Specific endonucleases release theoligonucleotides containing damaged bases;DNA polymerase and ligase fill and reseal thegap
Xeroderma pigmentosum |
single strand DNA repair
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Base excision repair
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Base-specific glycosylase removes altered baseand creates AP site (apurinic/apyrimidinic).One or more nucleotides are removed byAP-endonuclease, which cleaves the 5′ end.Lyase cleaves the 3′ end. DNA polymerase-βfills the gap and DNA ligase seals it.
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single strand DNA repair
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Mismatch repair
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Newly synthesized strand is recognized,mismatched nucleotides are removed, occurs in G2
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single strand DNA repair |
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mRNA start codons
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AUG
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mRNA stop codons
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UGA, UAA, UAG
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