Week 2 Richter Lectures Flashcards

1
Q

a group of genes, regulated together by transcription from a single promoter that produces polycistronic mRNA

A

operon

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2
Q

repressor binds to operator= what to transcription

A

inhibits

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3
Q

what is used to break down lactose

A

lac operon (found in prokaryotes)

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4
Q

Trp bound to repressor causes what to transcription

A

inhibits (Trp operon-found in prokaryotes)

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5
Q

acetylation of histones does what

A

turns on gene expression

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6
Q

methylation of histones does what

A

turns off gene expression (silences it)

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7
Q

what often happens to cancer (acetylation and methylation example)

A

oncogenes need to be methylated (to silence the gene)

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8
Q

drug used in anti-cancer chemotherapy that can reverse gene silencing, reduce proliferation, and trigger apoptosis

A

Vorinostat (drug that inhibits HDAC)

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9
Q

remove acetyl groups from chromatin, which often silences gene expression

A

histone deacetylases (HDACs)

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10
Q

what happens when gene expression is activated that should instead be silenced

A

cancer

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11
Q

if these get methylated, they won’t be able to stop cancer

A

tumor suppressors

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12
Q

3 functions of transcription factors

A
  1. DNA binding domain
  2. dimerization domain
  3. activation domain
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13
Q

a DNA-binding domain that allows TFs to insert themselves into grooves of DNA; Cys or His residues bound to Zn2+

A

Zinc finger

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13
Q

what receptors are basically transcription factors

A

nuclear receptors

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13
Q

DNA binding domain that has + and - charge by ionic interaction

A

basic domain

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13
Q

mutation of Vitamin D receptor leading to vitamin D deficiency

A

Rickets

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13
Q

mutation in thyroid hormone receptor leads to low T3 and thyroxine

A

Hypothyroidism

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13
Q

mutation of cortisol receptor leading to high levels of corticosteroids

A

Cushing’s Disease

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13
Q

nuclear receptor used in birth control (combination of 2)

A

estrogen/progesterone

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14
Q

mutation of retinoic acid receptor; can cause developmental defects in embryo and fetus

A

retinoic acid derivatives

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14
Q

used for acne and is contradicted during pregnancy

A

retinoic acid

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15
Q

2 dimerization domains

A

leucine zipper and HLH (helix-loop-helix) domain

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16
Q

All transcription factors are what

A

dimers

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17
Q

leucine residues are where on the helix (for leucine zipper)

A

on the same face

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18
transcription factor class that control fundamental architectural plan of developing embryo
helix-turn-helix (from Hemeobox (Hox) genes)
19
key process in gene silencing and defense against viral infections
RNA interference (RNAi)
20
main player in RNA interference (gene silencing)
miRNA
21
activates and cleaves mRNA during miRNA synthesis and gene silencing
RISC (RNA induced silencing complex)
22
regulated process during gene expression that results in a single gene coding for multiple proteins
alternative splicing
23
atleast one specific what is required per amino acid during translation
tRNA
24
what is the form of tRNA ready to be used in translation; and connects to amino acid
aminoacyl-tRNA
25
used as a signal initiation of translation; how the cell knows this RNA needs to be translated
7-methyl guanosine cap
26
a longer polyA tail means what for translation
most likely to happen
27
Initiation step of translation:
1. binding of methyl cap 2. joining of elF4B 3. 43S complex 4. joining of 60S with 43S at start codon (starts when it hits its first AUG)
28
elongation of translation sites:
A: recruits incoming aminoacyl tRNAs P: growing tRNA (from P to A) E: exit site (for empty tRNA)
29
many mRNAs have multiple _____ bound that allows translation of many proteins
ribosomes
30
this happens when the release factor enters the A site
termination of translation
31
this antibiotic binds to 30S subunit and causes misreading of genetic code; also inhibits initiation
aminoglycoside (streptomycin/gentamicin)
32
this antibiotic binds to 30S acceptor site (A site) and is just in the way
tetracycline
33
this antibiotic binds to 50S subunit and inhibits peptide bond formation
chloramphenicol
34
this antibiotic binds to 50S and blocks transferase reaction (inhibits enzyme that catalyzes formation)
erthromycin
35
this antibiotic binds to A site and acts as peptidyl acceptor- aborting elongation (blocks elongation)
puromycin
36
what blocks translation by inhibiting mTOR (mammalian target of rapamycin); inhibiting elF4E inhibits translation; also prevents blood vessel walls from thickening after angioplasty
rapamycin
37
addition/removal of AA's through signal sequence(marks protein for secretory pathway)/ubiquitination (degradation by proteasome)
post-translational modification
38
4 steps of post-translational modification
1. add/remove AA's 2. add carbohydrates 3. add lipids 4. reversible regulation through chemical modifications
39
what post-translational modification is essential for proper protein folding
N-glycosylation
40
addition of lipids to protein through post-translational modification
myristylation
41
amino acids used in phosphorylation during post-translational modification
Ser Thr Tyr
42
amino acids used in hydroxylation during post-translational modification
pro lys
43
methylation of histones
inhibits transcription
44
acetylation of histones
promotes transcription
45
lowers energy required for transition state (free energy of activation); increases rate of rxn
enzyme
46
rxn speed is increased dramatically when you introduce more ____
substrate
47
this alters enzyme activity and is different in different areas of the body
pH
48
extreme temperatures (high and low) do what to enzymes
inactivate them
49
substrate concentration at 1/2 vmax; similar to ligand concentration needed to occupy 50% of binding sites Measure of AFFINITY
Km; Kd
50
rxn speed is proportional to substrate concentration
first order
51
independent of substrate concentration
zero order
52
drug that competes with HMG-CoA (substrate at the active site); more drug than substrate leads to enzyme activity reduced
statin
53
shift of curve to the right (Km increases-add more substrate to get back to Km)
competitive inhibition
54
inhibitor does not compete with substrate at binding site; amount of active enzyme has decreased (vmax decreases)
noncompetitive
55
example of noncompetitive inhibitor
lead
56
lead being a noncompetitive inhibitor of ferrochelatase impairs heme synthesis and leads to what
anemia
57
inhibitor only binds to enzyme-substrate complex; vmax and Km decrease
uncompetitive enzyme inhibition
58
example of uncompetitive inhibitor (immunosuppressant); inhibits IMP dehydrogenase (B and T cells use this process)
mycophenolate
59
similar to noncompetitive; vmax decreases and Km stays the same
irreversible inhibition
60
organophosphorus pesticides leads to inhibition of acetylcholinesterase= SLUDGEM
irreversible inhibition
61
(drug) proton pump inhibitor; type of irreversible inhibition
omeprazole
62
can change Vmax or Km
allosteric regulators
63
AMP, GMP, IMP are heterotropic what
allosteric inhibitors
64
if IMP, GMP, and AMP are abundant in the cell; what feedback happens
negative
65
how cells even out substrates and products
+ and - feedback loops
66
what reduces DNA synthesis and explains toxicity of increased levels of dATP in adenosine deaminase deficiency
binding of dATP to allosteric sites on enzyme inhibiting enzyme activity
67
all CK in the brain is what isoform
BB
68
all CK in skeletal muscle is what isoform
MM
69
in cardiac muscle, 1/3 of CK is ___ and the rest is_____
MB; MM
70
enzyme indicator that cardio conversion (after myocardial infarction) was successful
MB (returns to normal value-decreases)
71
antibiotic that binds at A site and acts as a peptidyl acceptor
puromycin