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*U want to check if donor has CMV in his blood.*DNA purified from the leukocytes of the patient is reacted in a mixture containing oligonucleotides specific for CMV DNA, thermostable DNA polymerase, and nucleotides. Repetitive cycles of heating and cooling are performed, and the reaction product is detected by gel electrophoresis.*Procedure?
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*CPR.*Remember CMV infections in transplant patients is a major concern.
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Which proofreading activity is critical in determining the accuracy of nuclear DNA replication and thus the base substitution mutation rate in humans?
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*3′ to 5′ exonuclease activity of DNA polymerase δ
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10% guanine, 40% cytosine, 30% thymine and 20%adenine . What is the most likely source of the nucleic acid in this sample?a)Bacterial Plasmidb)Mitochondrial DNAc)Nuclear DNA of humand)Herpes virus 1 e)Herpes Virus 2f)Picornavirus g)Parvovirus
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*Answer is G)Parvovirus...All other choices have DOUBLE-STRANDED DNA composition which should obey the Chargaff's rule's (%A = %T, %C = %G), so we are left with SINGLE-Stranded agents like Picornavirus and Parvovirus but best choice would be parvovirus because it is Single-stranded but DNA virus, while picornavirus is Single-Stranded RNA virus(Nucleic acid sample would contain Uracil instead of thymine)Integrations maaan integration is the key ;)
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*Fluroqinolones(Floxacins) inhibit which prokaryotic enzyme necessary for bacterial DNA replication?
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*Topoisomerase II(DNA gyrase)<Normally it would unwind supercoils...Fluroquinolones also inhibit Topoisomerase IV which is involved in keeping sister chromatis separated from each-other.
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*RNA dependent DNA polymerase required for chromosome duplication in the nuclei of rapidly dividing cells, what enzyme it is, some conditions that might hint you that they talk about this enzyme?
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*Enzyme best fits description of TELOMERASE-they would talk about research involving Aging of human cells, Immortal cancer cells and some experimental treatments of cancers involving this enzyme, also they can talk about diseases that invovle defective Telomerase enzymes conditions like :Dyskeratosis congenital,PROGERIA, CONGENTIAL APLASTIC ANEMIA(I know for fact that last one has been tested and the answer was TERT gene mutation-which affects RNA components of Telomerase enzymes)
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Which class of enzyme catalyses the formation of the phosphodiester bonds in DNA repair?Damage is often due to Single-stranded breaks in DNA induced by free radicals damaging sugar-phosphage backbone.
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*DNA Ligases are the ones that seal them back together by forming phosphodiester bonds, while polymerases form phosphodiester bonds during DNA synthesis, Ligases are main players in REPAIR.
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*Mutation of cytoplasmic enzyme.*Mutation involves substitution of alanine for the serine(Normally present at position 127).*How this mutation results in decreased activity of the enzyme?
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*By PREVENTING Phosphorylation of the enzyme.
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3>5 direction:Strand-GCAGC5>3 direction:Strand CGTCGhow can you find mRNA?
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2 ways really, easier one would be just find 5>3 direction strand(CODING Strand) and the mRNA would be identical of course with exception of Thymidines-you just have to substitute Uracil for thymidines, but here we don't even have thymines so mRNA would be exac copy of CGTCG.*Alternative way is to find RNA complementary strand for Templade strand(GCAGC-you'd get same answer)
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*Transciption of genes by polymerase I vs*Polyadenylation of pre-mRNA by poly A polymerase?places?
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 *NucleoLUSvs*Nucleoplasm(part of nucleus outside the nucleolus) |
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UAC codes for tyrosineThey ask what codon could code for same amino-acid.why answer could be UAU but NOT UAA
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*Well it could be UAU because, wobble codons often differ ONLY in THIRD base, UAA wouldn't be the correct answer because it is a STOP codon(And yes you should know all stop codons-UAA,UGA,UAG)
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What is COMPLETE giveaway for I-cell disease? it can mimic Pompe disease, but when you see this phrase you pick Icell....
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*ELEVATION of lysosomal enzymes in the freakin SERUM.remember enzyme deficient here is Golgi-associated phosphotransferase(Defect is in POST-TRANSlational modification particularly PHOSPHOrylation of MANNOSE residuses,thus transport trough GOLGI is defective).
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Decreased secretion of the particular protein from the cell and its accumulation in the cytoplasm is suggestive of?mutation in which part of the gene that codes for that protein?
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*FIRST EXON which codes for the N-terminal amino acid signal sequence required for targeting of nascent protein to the ER(Likely defect here is translocation of nascent protein to ER)
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*What would you want to measure in tissue to identify if it is rich in Collagen?Note collagen is very rich in glycine....
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*You would want to check for something more unique to collagen and that would be something like HYDROXYproline(Remember hydroxylation of proline,lysine needs vitamin C, hence deficiency>Weak collagen)
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*X-linked Recessive Disease that causes FUNCTIONAL copper deficiency>Decreased acitivty of LYSYL oxidase which needs copper as cofactor>poorly cross-linked connective tissue>Fragile Bones/Blood vessels?
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*description best fits MENKES disease which is due to defective ATP7A(Don't confuse this with ATP7B defective in wilson), defective menkes protein(ATP7A)leads to defective transport/absorption of copper(Happens in STOMACH/Duodenum)>Decreased lysyl oxidase activity.(Copper is CoFactor for this enzyme)<>Can't cross link TROPOcollagen in ECF to make Collagen.Growth retardation/Hypotonia/brittle hair are other prominent signs often present with this diseasetreatment is IV copper.
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*Splice-site mutation?significance?
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*Base substitution at an intron-exon junction, which leads to the deletion of an entire exon and RETENTION of INTRON in mRNA, this can cause B-thalassemia,dementia,epilepsy and even cancer.
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