UCI SOM Lee
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| Helicase | MCM 2-7; opens the DNA helix; hexameric ring, uses ATP
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| Polymerase alpha | primer polymerase; lays down RNA primer for okazaki fragment binding
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| Polymerase beta | involved in BER
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| Polymerase gamma | mitochondrial DNA
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| Polymerase delta | lagging strand nuclear DNA
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| Polymerase epsilon | leading and lagging strand nuclear DNA
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| Polymerases with proofreading ability | gamma, delta, epsilon
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| Sliding clamp | PCNA
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| Clamp loader | RF-C
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| Single strand DNA binding protein | RPA
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| DNA ligase | Ligase I
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| DNA topoisomerase | Topo I and II
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| RNase H | removes all but one ribonucleotides
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| FEN1 | removes last ribonucleotide and several deoxynucleotides
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| Contributing factors to high fidelity DNA replication | polymerase, exonuclease proofreading, MMR
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| Are polymerization and editing activity located at the same site on the pol | NO
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| Do all DNA pols have 3’ to 5’ exonuclease activity | NO
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| DNA ligase action | seals 3’OH and 5’Phosphate
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| What does processivity mean | how many nucleotides are added in one attachement
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| Which enzyme is responsible for telomere length maintenance | telomerase
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| Human telomerase | hTERT-human telomere reverse transcriptase
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| What proteins recognize mispairs, small deletions, and small insertions in MMR | MSH heterodimer
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| What proteins make MMR cleavage | PMS2
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| How are newly synthesized strands detected | lagging strand has gaps; leading strand I don’t have a clue
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| Examples of epigenetic change | hypermethylation of CpG island; post-translational modification of a histone; repair gene is transcriptionally silenced through epigenetic modification
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| 8-oxoG is repaired by | BER
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| BER steps | glycosylase cuts out the damaged base, AP endonuclease cleaves the deoxyribose phosphate backbone, AP lyase binds it all up
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| Y-family DNA pols | used for DNA synthesis when template is damaged; pol eta is in this family and it’s mutation leads to XPV
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| DNA topo I | introduces a single stranded break; attached to 3’ of DNA
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| DNA topo II | introduces a double stranded break; needed for daughter chromosome separation
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| Campothecin | drug that reversibly binds and stabilizes cleavable complexes formed between DNA and topo I; used in cancer treatment
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| Doxorubicin | inhibits topo II; widely used in breast cancer treatment; also known as adriamycin
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| Replication origin | discrete sit on chromosome where replication starts
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| Fusion of S and G1 cells results in | DNA synthesis inducement in G1
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| Fusion of G2 and S cells results in | no change
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| Telomore DNA sequence | TTAGGG
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| Diseases caused by trinucleotide repeat expansion | fragile X syndrome, friedreich’s ataxia, myotonic dystrophy, spinocerebellar ataxia type B, huntington’s disease, kennedy’s disease
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| Huntington’s disease | expansion of CAG repeat
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| Spontaneous DNA damage | base loss (mostly purines), tautomeric shift (keto to enol or amino to imino), deamination, ROS damage (mostly in mitochondria, alkylation lesions
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| Environmentally induced DNA damage | UV damage (260 nm) eg thiamine dimmers (CPD) and 6-4PP, chemicals
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| 4 other types of DNA damage | replication errors, intra and inter strand crosslinks, DNA-protein crosslinks, strand breaks
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| types of DNA repair | photolyase, alkyltransferase, BER, DER, MMR
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| photolyase | reverses UV damage; not present in humans
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| alkyltransferase | removes methyl group from O6 position of guanine; the repair protein is AGT which is the same as MGMT
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| AGT | O6-alkylguanine-DNA alkyltransferase (used in alkyltransferase)
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| MGMT | O6-methylguanine-DNA methyltransferase (used in alkyltransferase)
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| O6-meG cell apoptosis process | requires MMR; MMR removes thymine which introduces a break in DNA; O6-meG also can bind to MutS which recruits ATR-ATRIP
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| BER short patch repair | dominant repair pathway; DNA pol beta fills one nucleotide
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| BER long patch repair | uses pol beta, delta and epsilon (2-10 bases), and PCNA. FEN1 removes DNA flap and ligase 1 seals the gap
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| 3 steps to BER | 1)N-glycosylase creates an AP site 2)AP endonuclease (APE) nicks at 5’ of AP site 3)extension by DNA pol
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| 3 genetic NER diseases | xenoderma pigmentosum, cockayne’s syndrome, trichothiodystrophy
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| xenoderma pigmentosum | light sensitivity, weird pigmentation, early skin cancer
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| cockayne’s syndrome | premature aging, dwarfism
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| trichothiodystrophy | premature aging, brittle hair, short, facial abnormalities
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| origins of DSB | IR, ROS, and replication of SSB
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| Rad 51-59 | basically facilitate in homology search
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| Rad 50 | process DNA at ends of a double stranded break
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| BRCA1 | deficient in breast cancer and interacts with Rad 50
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| BRCA2 | breast cancer susceptibility gene and interacts with Rad 51`
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| DNA damage checkpoints | G1 checkpoint is leaving G1 and going to S, G2 checkpoint is leaving G2 and going into M, Metaphase checkpoint assures all chromosomes are attached to spindles
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| DNA damages repaired by BER | c deamination, 8-oxoguanine, single strand break
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| DNA damages repaired by NER | 6-4PP, bulky adduct, CPD (T-T dimmer)
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| DNA damages repaired by recombination repair | interstrand cross-link, double strand break
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| DNA damages repaired by MMR | A-G mismatch, T-C mismatch, insertion, deletion
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| Damages repaired by BER | x-rays, ROS, alkylating agents, spontaneous rxns
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| Damages repaired by NER | UV, polycyclic aromatic hydrocarbons
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| Damages repaired by recombination repair | x-rays, anti tumor agents
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| Damages repaired by MMR | replication errors
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| MMR subunits | MutSalpha (MSH2-6) recognizes the MM and interacts with PCNA; MLH1-PMS2 has endonuclease activity
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| MSH2-6 | recognizes a mismatch for MMR
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| PMS2-MLH1 | makes the cut in MMR
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| FAP and what gene is mutated | familial adenomatous polyposis; APC is mutated
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| Asbestos can lead to what | mesothelioma
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| Inhaling cigarette smoke can lead to what | G to T transversion
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| Futile DNA repair models | add extra DNA sequences when cell is not dividing
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| DNA translesion | DNA replication using a Y-family polymerase b/c there are too many mutations to use pol delta/epsilon
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