Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Biochem > molecular > Flashcards

molecular Flashcards

1
Q

nucleosome

A

H2A, H2B, H3, H4 - two of each.
POSITIVELY CHARGED.

negative DNA loops twice around each octamer. octamer subunits are mainly LYS and ARG.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

histone H1

A

ties nucleosome “beads” together.

ONLY histone that is not in nucleosome core.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

HeteroChromatin

A

Highly Condensed.
transcriptionally inactive.
sterically inaccessible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

methylation

A

template strand CYTOSINE and ADENINE are methylated during DNA replication, allowing mismatch repair enzs to distinguish old and new strands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

HYPERmethylation

A

inactivates DNA transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

euchromatin

A

less condensed.
transcriptionally ACTIVE.
sterically accessible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

histone acetylation

A

relaxes DNA coiling,

allows for transcription.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

deamination of what base makes uracil?

A

cytosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

guanine contains?

A

ketone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

thymine contains?

A

methyl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

which bonds are stronger?

A

G-C (3 H bonds)

vs. A-T (only 2 H bonds)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

increased G-C content means..?

A

increased melting temp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

AA needed for PURINE synth?

A

Glycine
Aspartate
Glutamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

nucleotides linked together by?

A

3’-5’ phosphodiester bonds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

AA needed for pyrimidine synth?

A

aspartate

only other component is carbamoyl phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

purine process

A
  1. start with sugar + phosphate (PRPP).

2. add base.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

pyrimidine process

A
  1. make temporary base (OROTIC ACID).
  2. add sugar + phos.
  3. modify base.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ribonucleotide reductase

A

convert ribonucleotides to deoxyribonucleotides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

carbamoyl phosphate

A

2 uses:

  1. de novo pyrimidine synth.
  2. urea cycle.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

if carbamoyl phosphate can’t be used for urea cycle…

A

due to deficiency of ornithine transcarbamoylase (OTC), carbamoyl phosphate ACCUMULATES and is converted to OROTIC ACID of pyrimidine pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

orotic aciduria

A

auto recessive inability to convert orotic acid to UMP (de novo pyrimidine synth).

due to defect of:

  1. orotic acid phosphoribosyltransferase (adds PRPP).
  2. orotidine 5’-phosphate decarboxylase (removes CO2 to form UMP.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

orotic aciduria FINDINGS

A

increased orotic acid in urine.
megaloblastic anemia.
failure to thrive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

orotic aciduria vs OTC deficiency

A

no hyperammonemia in orotic aciduria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

TX of orotic aciduria

A

oral uridine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is significant about megaloblastic anemia of orotic aciduria?

A

does NOT improve with admin of B12 or folic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

adenosine deaminase

A

convert adenosine to inosine in purine salvage pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

adenosine deaminase deficiency

A

excess ATP and dATP imbalance via feedback inhib of ribonucleotide reductase
= prevent DNA synth and thus, decrease lymphocyte count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

adenosine deaminase deficiency causes what disease?

A

SCID:
B and T cells die off.
occurs in kids.
1st to be treated with experimental human gene therapy (retroviral vector).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Lesch Nyhan syndrome

A

defective purine salvage due to absent HGPRT.

results in excess uric acid prod and de novo purine synth.

X-linked recessive.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

HGPRT

A

converts hypoxanthine to IMP,

guanine to GMP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Lesch Nyhan syndrome FINDINGS

A 
retardation.
self mutilation.
aggression.
hyperuricemia.
gout.
choreoathetosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the only base that can be salvaged in Lesch Nyhan syndrome ?

A

adenine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

genetic code feature: unambiguous

A

each codon specifies only ONE AA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

genetic code feature: degenerate/redundant

A

more than 1 codon may code for SAME AA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

genetic code feature: commaless, nonoverlapping

A

read from a fixed starting point as a continuous sequence of bases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

AA that are NOT degenerate/redundant

A

methionine (AUG) and tryptophan (UGG) are encoded by only ONE codon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

genetic code feature: universal

A

genetic code is conserved throughout evolution (except: mito DNA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

severity of DNA mutations

A

nonsense > missense > silent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what do frameshift mutations often result in?

A

truncated, nonfunctional protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

where does DNA replication begin in prokaryotes?

A

at consensus sequence of base pairs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

where does DNA replication begin in eukaryotes?

A

multiple consensus points (origins of replication)

42
Q

helicase

A

unwinds DNA template at replication fork

43
Q

single-stranded binding proteins

A

prevent strands from reannealing

44
Q

DNA topoisomerases

A

create nick in helix to relieve supercoils created during replication

45
Q

DNA gyrase

A

PROKARYOTIC
topoisomerase II.

*inhibited by fluoroquinolones

46
Q

primase

A

DDRP.

makes RNA primer on which DNA pol III can initiate replication.

47
Q

DNA polymerase III

A

PROK ONLY.

  1. elongates leading strand by adding deoxynucleotides to the 3’ end (5’-3’ synth).
  2. elongates lagging strand until it reaches primer of preceding fragment.
  3. 3’-5’ exonuclease activity to proofread each added nucleotide.
48
Q

DNA polymerase I

A

PROK ONLY.

  1. degrades RNA primer with 5’-3’ exonuclease.
  2. fills in gap with DNA (5’-3’ synth).
  3. proofreads with 3’-5’ exonuclease activity.
49
Q

DNA ligase

A

seals

50
Q

telomerase

A

adds DNA to 3’ end of chromosomes to avoid loss of genetic material with each duplication

51
Q

nucleotide excision repair

A

single strand.

specific ENDONUCLEASES release oligonucleotide-containing damaged bases.

DNA pol fills gap, ligase reseals.

52
Q

xeroderma pigmentosum

A

endonuclease deficiency.

UV light causes THYMINE DIMER formation.
UV endonuclease needed to excise dimer.
deficiency = inability to repair.

53
Q

features of XP

A

photosensitivity.
poikiloderma.
hyperpigmentation.
increased risk for skin cancer.

54
Q

base excision repair

A

single strand.

specific GLYCOSYLASES recognize and remove damaged bases.

AP endonuclease cuts DNA at apurinic or apyrimidinic site, empty sugar removed.

gap filled and resealed.

55
Q

base excision repair is important for?

A

repair of spontaneous or toxic deamination

56
Q

mismatch repair

A

single strand.

unmethylated, newly synthesized string is recognized. EXONUCLEASE removes mismatched nucleotides.

gap filled and resealed.

57
Q

mutated mismatch repair

A

HNPCC: hereditary nonpolyposis colorectal cancer

58
Q

nonhomologous end joining

A

double strand repair.
brings 2 ends of DNA fragments together.
homology not required.

59
Q

mutated nonhomologous end joining

A

ataxia telangiectasia

60
Q

rRNA

A

made by EUK RNA pol I.
most abundant type.
“Rampant”

61
Q

mRNA

A

made by EUK RNA pol II.
longest type.
“Massive”

62
Q

tRNA

A

made by EUK RNA pol III.
smallest type.
“Tiny”

63
Q

mRNA start codon

A

AUG:
codes for methionine in EUK.
formyl-methionine (f-Met) in PROK.

*starts PROTEIN synth.

64
Q

mRNA stop codons

A

UGA
UAA
UAG

65
Q

promoter

A

site where RNA pol and multiple other TFs bind DNA upstream of gene locus.

AT-rich sequence with TATA and CAAT boxes.

66
Q

mutated promoter

A

dramatic decrease in amount of gene transcribed

67
Q

enhancer

A

stretch of DNA that alters gene expression by binding transcription factors

68
Q

silencer

A

site where negative regulators (repressors) bind

69
Q

where are enhancers and silencers located?

A

anywhere….

close to, far from, or even within the gene whose expression is being regulated

70
Q

RNA polymerases

A

no proofreading.

can initiate chains.

71
Q

PROK RNA pol

A

only 1 type. multisubunit complex.

makes all 3 kinds of RNA.

72
Q

which EUK RNA pol opens DNA at promoter site?

A

RNA pol II

73
Q

what toxin can inhibit RNA pol II?

A

alpha-amanitin (amatoxin) in death cap mushrooms - stops mRNA synth.

cause liver failure if ingested.

74
Q

hnRNA

A

heterogeneous nuclear RNA (initial transcript) - must be processed before it can leave nucleus

75
Q

RNA processing

A
  1. 5’ cap (7-methylguanosine).
  2. 3’ polyadenylation (200 A’s).
  3. splicing of introns.

= mRNA

76
Q

Abs to spliceosomal snRNP

A

lupus

77
Q

lac operon: allolactose

A

inhibits repressor

78
Q

lac operon: glucose

A

inhibits activator

79
Q

exons

A

contain actual genetic info coding for protein

80
Q

introns

A

intervening noncoding segments of DNA

81
Q

alternative splicing

A

combines diff exons to make unique proteins in different tissues

ex: beta thal (abn splicing)

82
Q

tRNA structure

A

75-90 nucleotides.

secondary structure: cloverleaf.

83
Q

tRNA 3’ aminoacyl end

A

contains CCA and high #chemically modified bases.

AA covalently binds to 3’OH of CCA tail.
“Can Carry Amino acids”

84
Q

tRNA charging

A

aminoacyl-tRNA synthetase (uses ATP) examines AA before and after it binds to tRNA

85
Q

what happens if AA-tRNA bond is incorrect?

A

bond is hydrolyzed

86
Q

where does energy for peptide bond formation come from?

A

AA-tRNA bond

87
Q

what blocks attachment of aminoacyl-tRNA to ribosome?

A

tetracyclines - bind 30S subunit

88
Q

tRNA wobble

A

accurate base pairing only required for FIRST 2 nucleotide positions of codon.

3rd WOBBLE position can code for same tRNA/amino acid.

89
Q

protein synth: initiation

A

activated by GTP hydrolysis.

initiation factors help.

90
Q

initiation factors (eIFs)

A

help assemble 40S subunit with initiator tRNA.

released when mRNA and ribosomal subunit assemble with complex.

91
Q

EUK ribosomal subunits

A

40S + 60S = 80S (Even)

92
Q

PROK ribosomal subunits

A

30S + 50S = 70S

93
Q

protein synth: elongation

A
  1. charged tRNA binds A site.
  2. ribosomal rRNA (RIBOZYME) catalyzes peptide bond formation, transferring growing polypeptide TO CURRENT AA in A site.
  3. ribosome advances 3 nucleotides toward 3’ of mRNA, moving growing peptidyl RNA to P site (translocation).
94
Q

protein synth: termination

A

stop codon recognized by RELEASE FACTOR.

completed protein released from ribosome.

95
Q

posttranslational modification: trimming

A

remove N or C-terminal PROpeptides from zymogens to create mature proteins

96
Q

posttranslational modification: covalent alterations

A

phosphorylation,
glycosylation,
hydroxylation

97
Q

posttranslational modification: proteasomal degradation

A

attachment of UBIQUITIN to defective proteins to tag them for breakdown

98
Q

aminoglycosides

A

bind 30S and inhibit formation of INITIATION COMPLEX.

cause misreading of mRNA.

99
Q

chloramphenicol

A

inhibit peptidyltransferase (ribosomal rRNA/ribozyme), AKA peptide bond formation.

binds 50S.

100
Q

macrolides

A

block translocation (A to P site)- prevent release of uncharged tRNA after it has donated its AA

Biochem (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions