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MCM Diseases > Exam 2 Quiz > Flashcards

Exam 2 Quiz Flashcards

1
Q

Cross-linking agents of DNA damage

A

Nick convinced me to cross dress

Nitrogen mustard, cisplatin, mitomycin C, carnestine

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2
Q

Alkylation agents of DNA damage

A

Dimethyl sulfate, methylmethanesulfate

DMS and MMS

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3
Q

Intercalating agents of DNA damage

A

Thalidomide (used to be for morning sickness, fits between grooves of DNA)

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4
Q

Competitive inhibitor of DNA polymerase (anti-leukemia drug)

A

Ara-C

Has no 3’ OH end

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5
Q

Introns start and end with

A

Start with GT and end with AG

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6
Q

Xeroderma pigmentosum

A

Defect in NER complex.
NER - 2 adjacent bases form a dimer. NER removes entire stretch and replaces

Melanomas and squamous cell carcinomas.

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7
Q

Hereditary nonpolyposis colorectal cancer

A

Autosomal dominant. Defect in MER complex (DNA repair gene faulty)

MER - Mut S binds while MutL scans for nicks and mismatches. Removes stretch on one strand and replaces fixing the mismatch.

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8
Q

Cockayne syndrome

A

Microcephalic, failure to thrive, photosensitivity

NER complex

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9
Q

BRCA breast cancer

A

Defect in tumor suppressor genes. Problem with homologous recombination (use sister chromatid to accurately repair)

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10
Q

Rifempcin

A

ABX that inhibits bacterial RNA synthesis, but has drug-drug interactions (warfarin, etc.)

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11
Q

CpG site deamination

A

5-methylcytosine to thymine (unsilences gene)

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12
Q

Start codon in genome and RNA

A

ATG and then AUG

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13
Q

Stop codons

A

UAA, UAG, UGA

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14
Q

Sickle cell anemia

A

Glutamine replaced by Valine

Neg charge and hydrophilic to hydrophobic

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15
Q

Ubiquination

A

C-terminal glycine recognizes lysine residues of target proteins. Then recognized by 26S proteosome and degrades target protein

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16
Q

TRNA

A

Adapter to bind both mRNA and AA

Has both Anticodon loop for mRNA and 3’ CCA terminal region for binding AA that matches the codon

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17
Q

Aminoacyl tRNA

A

tRNA and AA complex. Catalyzed by aminoacyl tRNA synthetases. Then binds to codon in RNA

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18
Q

Eukaryotic ribosomal unit

A

60S and 40S

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19
Q

Prokaryotic ribosomal unit

A

50S and 30S. Often used by antibiotics to target translational machinery

20
Q

Initiator complex in eukaryotes

A

Methioninyl tRNA

goes onto small subunit of ribosome at p-site

21
Q

Release factors

A

Bind to A site in response to stop codons. Cleave the ester bond between C terminus of polypeptide (end) and the tRNA

22
Q

Tetracycline

A

Binds to prok small 30S subunit, blocking entry of aminoacyl tRNA

23
Q

Chloramphenicol

A

Inhibits peptidyl transferase (prok)

24
Q

Clindamycin and Erythromycin

A

Binds to large 50S subunit (prok) blocking translocation of the ribosome

25
Q

Streptomycin

A

binds to 30s subunit and interferes with fmet-tRNA binding. Also affects the 50S/30S binding (prok)

26
Q

Cyclyheximide

A

Inhibits peptidyl transferase (euk)

27
Q

Diphtheria toxin

A

Inactivates GTP bound EF-2, interfering with ribosomal translocation

28
Q

Shiva toxin

A

binds to 60S, blocking entry of aminoacyl tRNA to ribosomal complex

29
Q

Puromycin

A

Causes premature chain termination (prok and euk). Looks like 3’ end of aminoacylated tRNA

30
Q

I-Cell disease (inclusion cell disease)

A

Tagging of mannose-6-phosphate is defective. High plasma levels of lysosomal enzymes - death usually around 7 years old

31
Q

Glycosylation

A

Either O-glycosidic (Ser or Thr) or N-glycosidic (Asparagine). Usually for extra cellular proteins

32
Q

Phosphorylation

A

Uses serine/threoenine and will either dephosphorylate or phosphorylate.

33
Q

Disulfide bond formation

A

2 cysteine residues (HS-SH). Done by protein disulfide isomerases

34
Q

Acetylation

A

Acetylated on lysine residues, using Acetyl Co-A as donor. HAT and HDAC

35
Q

Collagen post translational modifications

A

Ascorbic acid essential for activity of Lysyl hydroxylase - Ehlers, Danlos, Nevo syndrome, and Epidermis Bullosa Simplex

36
Q

Alzheimer’s disease

A

Amyloid precursor protein into Amyloid beta peptide, which form plaques. Also hyperphos of Tau (intracellularl) cause familial form of AD

37
Q

Parkinson’s

A

Alpha-synuclein (AS) forms Levy bodies in dopaminergic neurons in substantial Nigra. Selective death.

38
Q

Huntington’s

A

CAG triplet repeats (polyglutamine repeats) cause misfolding and aggregating. Selective death of Basal ganglia cells

39
Q

Creutzfeldt-Jakob disease

A

Misfolding of prions. Transmissible. Converts normal into misfolded. Belongs to TSEs to form spongy appearing parts of brain

40
Q

Gs G protein

A

Stimulates adenylate cyclase to make cAMP, which activates PKA to phosphorylate target proteins. Stimulated by histamine and epi

41
Q

Gi G protein

A

Inhibits adenylate cyclase, no PKA activity. Stimulated by dopamine

42
Q

Gt G protein

A

Stimulates cGMP PDE to convert cGMP to 5’ GMP. Turns off already active signal. Stimulated by light

43
Q

Gq G protein

A

Activates phospholipase C, which turns PIP into IP3 and DAG.

IP3 activates Ca2+ channels on SR/ER to activate Ca2+ dependent proteins

DAG and IP3 activates PKC, which phosphorylates target proteins.

Stimulated by acetylcholine

44
Q

Cholera

A

Ribosylation of Arginine, leads to decrease in GTPase activity, but Gsalpha continues to stimulate AC and overproduction of cAMP occurs (which activates CFTR). This opens CL- channels and loss of electrolytes and water via diarrhea

45
Q

Pertussis

A

Ribosylation of Cys on Gialpha. Prevents activation and dissociation of alpha subunit from Beta and gamma. Less inhibition of AC, overproduction of cAMP. Loss of fluid and excessive mucous in epithelial cells.

MCM Diseases (3 decks)

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