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Cmcb > Final review CMCB > Flashcards

Final review CMCB Flashcards

1
Q

Li-Fraumeni syndrome

A

one p53 allele eliminated in germ line
later somatic cell mutations in any tissue causes tumor
multiple, numerous cancers
autosomal dominant inheritance

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2
Q

angelman syndrome

A

gene known as UBE3A is either absent or malfunctions

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3
Q

Papillomavirus

A

warts
carcinoma of the uterine cervix
smoking, HIV
DNA virus

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4
Q

Hepatitis B virus

A 
liver cancer (hepatocellular carcinoma), aflatoxin, alcoholism, smoking
DNA virus
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5
Q

Hep C virus

A 
liver cancer (hepatocellular carcinoma)
DNA virus
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6
Q

Epstein-Barr virus

A

Burkitt’s lymphoma (cancer of B lymphocytes)
nasopharyngeal carcinoma
malaria
DNA virus

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7
Q

Human T-cell leukemia virus type I (HTLV 1)

A

adult T-cell leukemia/lymphoma

RNA virus

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8
Q

HIV virus

A

RNA virus
Kaposi’s sarcoma,
other viruses

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9
Q

causes of cancer

A

retrovirus, carcinogen, gamma irradiation, chromosomal translocations

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10
Q

what is myasthenia gravis

A

autoimmune disorder; antibodies fight and destroy acetylcholine receptors needed for muscle contraction.

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11
Q

what docks into major groove?

A

alpha helix
beta hairpin
protein

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12
Q

side chain of Asn or Gln recs

A

N6 and N7 of adenosine base

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13
Q

side chain of Arginine recs

A

06 and N7 of guanine

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14
Q

what is helix turn helix motif found in

A

prokaryotes and bacteriophages, form homodimers

second helix is recognition helix

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15
Q

homeodomain

A

eukaryotic transcription factors; three consecutive alpha helices, third one docs into major groove

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16
Q

zink fingers

A

eukaryotes, one or more zinc atoms. most common in eukaryotes. beta hairpin and recognition alpha helix.

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17
Q

leucine zipper

A 
eukaryotes;
two alpha helices
recs DNA at N terminal
dimerize at C terminal 
homodimers
heterodimers/ asymmetries
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18
Q

two types of loop and strand motifs

A

beta-hairpin recognition

helix and loop recognition

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19
Q

what activates lac operon

A

Catabolite Activator Protein

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20
Q

what are the four lac operon cases

A
    • glucose + lactose, CAP not bound, operon off
    • glucose - lactose; repressor bound; operon off
  3. -glucose -lactose; CAP bound to activator with cAMP, but repressor bound; lac operon off
  4. -glucose + lactose; repressor not bound, CAP bound with cAMP; CAP recruits polymerase and operon on
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21
Q

p53

A

tumor suppressor; mutations in cancer localize to protein DNA interface and weaken ability of p53 to bind to DNA

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22
Q

modular design of gene activator proteins

A

simplest have two modules

  1. DNA binding domain
  2. activation domain; initiates transcription with transcription factors, Mediator and/or APol II
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23
Q

concept ot transcriptional synergy

A

when activators bind together, effects can be multiplicative, not additive

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24
Q

insulator regulation

A

enhancer elements betweeen two genes might activate both,m but an insulator element can block one of the genes from enhancer if it places itself between gene and enhancer

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25
Q

architectural proteins

A

bend DNA, bringing proteins on either side of the bend close togtether to mediate interactions to either repress or activate

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26
Q

four ways to change histone code

A
  1. ATP dependent chromatin remodeling complexes decondenses
  2. histone chaperones remove histones to make DNA accessible
  3. modified histones swapped for unmodified one
  4. HATs acetylate histone tail proteins to alter code
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27
Q

how does histone acetyltransferase work

A

acetylate histone lysine residues. replaces positive amine group of lysine side chain with neutral acetyl group and reduces positive charge. activates transcription.

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28
Q

histone deacetylases (HDACs)

A

remove neutral acetyl group from modified lysine residues, leaving behind a positively charged amine. increases positive charge of histone. represses activation.

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29
Q

Ser/Tyr phosphorylation and dephosphorylation

A

adds negative charge. activates?

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30
Q

lysine methylation and demethylation

A

methylation represses activation

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31
Q

methylation in vertebrates

A

limited to 5 position on cytosine base, major groove

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32
Q

fragile x synderome

A

x linked dominant
epigenetic
inherited mental retardation

decreased or absent levels of fragile X mental retardation protein. loss of function in FMR1 gene. expanded CGG repeats in 5’ UTR of gene that silences expression.

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33
Q

prader-willi syndrome

A

neurodevelopmental disorder. characterized by obesity, hypogonadism, and mid to moderate mental retardation

paternal cytogenetic deletion at 15q11-q13

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34
Q

angelman syndrome

A

maternal cytogenetic deletion at 15q11-q13
UBE3A gene causes syndrome.

childhood epilepsy, severe developmental delay and happy demeanor with excessive laughter

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35
Q

long noncoding RNA (lncRNA)

A

Xist lncRNA example; inactivate X chromosome, coats chromosome

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36
Q

RNA editing by alternate splicing

A

controled by RNA binding proteins.
negative control: repressor molecule binds to a splice juntion and buries site
positive control: splicing activator binds to enhancer element

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37
Q

stimulated vs. nonstimulated B lymphocyte

A

stimulated: CstF, expression; earlier 3’ cleavage site; polyadenylated. shorter, missing hydrophobic tail so secreted.
nonstimulated: membrane bound because of hydrophobic tail. full length. longer

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38
Q

when does RNA editing happen

A

after transcription

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39
Q

adenosine d: eaminases

A

act on RNAs (ADARs) carry out A to I editing. A pairs with U. I pairs with C. causes Gln –> Arg mutation in transmitter gated ion channel in brain

C to U editing; deamination ApoB-100 liver , intesting editaed from CAA to UAA stop codon, shorter ApoB 48.

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40
Q

iron starvation conditions

A

NEED IRON
transferrin receptor translation activated: recruiters iron bound to transferrin into the cell.
Storage of excess iron in ferritin not needed.
aconitase: turns on transferrin by binding to i3;UTR of it to prevent endonucleolytic cleavage. shuts off translation of ferritin by binding to 5;UTR of ferritin .

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41
Q

excess iron

A

aconitase detaches from transferrin rerceptor mRNA to allow endonucleolytic cleaveage and thus inactivation. to activate ferritin, excess iron binds to aconitase so it dissociates from 5;UTR of ferritin mRNA to permit initiation of translation.

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42
Q

internal ribosome entry sites (IRESs)

A

occur anywhere within gene

uses different proteins than CAP dependent translation. IRES RNA is folded. IRES bypasses CAP recognition.

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43
Q

IRESs in viral translation

A

require eIF4G but not eIF4E. both host and viral RNAs are translated. viral protease to remove part of eIF4G, which blocks binding to eIF4E. then non-IRES dependent translation is inhibited.
cleavage means virus gets translated

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44
Q

miRNA

A

micro RNA
act as tumor suppressors and oncogenes
mir21 significantly upregulated in many malignancies

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45
Q

key oncogenes

A

c=Myc, Ras, Her2, EGFR, Bcr-Abl

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46
Q

SDS page

A

separates protein based on size

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47
Q

CRISPRs

A

clustered regularly interspaced short palindromic repeats
DNA loci containing short repetitions of base sequence

CRISPRs/Cas9 system used for gene editing. Use Cas9 protein and guide RNA to cut genome at desired location.

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48
Q

wild type Cas9

A

specifically cleaves ds DNA activating ds break repair machinery.

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49
Q

mutated Cas9

A

site specific single strand nick.

50
Q

nuclease deficient Cas9

A

fused with various effector domains allowing specific localization

51
Q

antisense therapy for spinal muscular atrophy

A

spinal muscular atrophy caused by loss of function mutation in SMN1 gene.

in SMN2 gene, a single nucleotide sub in exon 7 interferes with an exonic splicing enhancer, impairing production of normal SMN protein. AOs tareted to the ntronic splice silencer site (ISS) in intron 7 facilitate the retention of exon 7 within the mature mRNA, increasing the production of functional SMN protein.

52
Q

Hallmarks of cancer

A
  1. sustaining proliferative signaling
  2. evading growth suppressors
  3. activating invasion and metastasis
  4. enabling replicative immortality
  5. inducing angiogenesis
  6. resisting cell death
53
Q

bcl-2

A

anti-apoptotic gene

54
Q

normal cell growth culture characteristics

A

a. substrate dependence for growth
b. serum dependence for growth
c. contact inhibition for growth

55
Q

calc total cell cycle

A

count no. of cells present and record number of hours it takes for the total number to double

56
Q

calculate: S phase

A

need labeling to measure

57
Q

cal m phase

A

cells scanned and fraction in mitosis is assayed

58
Q

to cal G1 and G2 phases

A

synchronize cells

59
Q

flow cytometer

A

cells with least DNA, G1
double this amt, G2 and M,
intermediate amount is S

60
Q

major players in determinism

A

S-phase activator (start kinase)
M-phase promoting factor (MPF)
cyclin
cyclin dependent kinase

61
Q

deterministic hypothesis

A

once cells pass a certain point in the cell cycle they are committed to continue through the cycle.
there exists a restriction in late G1 called START (in yeast).

62
Q

dk

A

associates successively with different cyclins to trigger different downstream processes of cycle. cdk activity terminated by cyclin degradation.

63
Q

S-Cdk

A

trigers DNA replication machinery

64
Q

M-Cdk

A

trigers mitosis machinery

65
Q

G1/S-cdk

A

triggers at G1/S border

66
Q

G1-Cdk complex cyclin and cdk partner

A

cyclin D and Cdk4 and 6

67
Q

G1/S-cdk

A

cyclin E and Cdk2

68
Q

S-Cdk

A

cyclin A and cdk2

69
Q

M-cdk

A

cyclin B and cdk1

70
Q

start MPF activity by M Phase Promoting Factor

A

cyclin B and CDK1 or 2

71
Q

Cdks activated by

A

cdk-activating kinase (CAK)

72
Q

inactivate cyclin/cdk complex

A

wee1 kinase phosph. cdc2’, inhibits dcd activity until phosphate removed by cdc 25 phosphataase

p27 inhibits cdk, blocks phosphate

73
Q

M phase cyclin and cdk

A

B/ cdk1

74
Q

G1 cyclin and cdk

A

d: cdk4/6

75
Q

S phase cyclin and cdk

A

A and cdk2

76
Q

g2 cyclin and cdk

A

A and cdk 1

77
Q

p16, p21, p27

A

inhibit cdk/cyclin

78
Q

Rb

A

retinoblastoma protein, a tumor suppressor protein, inhibits regulatory protein

79
Q

basics of oncogenesis

A

a. overactivity mutation by gain of function (single mutation event)
b. underactivity mutation (loss of function): tumor suppressor gene stopped by two inactivating mutations

80
Q

src

A

oncogene, part of small RNA genome of Rous sarcoma virus, a retrovirus
protein tyrosine kinase that binds to cell’s PM and phosphorylates cellular proteins converting cell to cancerous growth

81
Q

RNA virus mechanism

A

viral RNA copies into ds DNAwith reverse transcriptase

RNA is transcribed with DNA

82
Q

DNA virus

A

viral DNA not integrated into host genome

83
Q

cancer agents of transformation (4)

A

viruses, chemicals, irradiation, chromosomal translocations and duplications

84
Q

aflatoxin

A

activated by cytochrome p450. indirect acting carcinogen . liver cancer. acts on 053 tumor suppressor protein.

85
Q

Burkitt’s lymphoma

A

reciprocal translocation bet ch. 8 and 14, malignancy of B B cells in human immune system. oncogene myc is activated. EBVirus promotes oncogenesis in burkitts. inhibits apoptosis in B cells.

86
Q

chronic myelogeous leukemia (CML)

A

philadelphia chromosome, fusion bet. BCR gene and ABL gene. fusion of ch. 9 to piece of ch. 22 to make 9q+ and 22q-.
Bcr/Abl fusion oncogene, protein tyrosine case is acvitated.

87
Q

gleevec

A

used for CML, active site inhibitor of Abl kinase activity,

88
Q

c-abl activation by fusion drives

A

excessive proliferation of a clone of hemopoietic cells in bone marrow
tyrosine kinase constitutive. c-abl is protooncogene

89
Q

oncogenes and oncoproteins

A 
growth factors
receptors
intracellular transducers
nuclear transcription factors
cell cycle control proteins
90
Q

erbB

A

truncated growth factor receptor

91
Q

sis oncogene

A

growth factor (PDGF)

92
Q

src oncogene

A

protein tyrosine kinase

93
Q

ras oncogene

A

GTP binding protein

94
Q

myc oncogene

A

transcription factor, cell cycle

95
Q

Rb

A

tumor suppressor

96
Q

two ways to convert protooncogene to an oncogene

A

dosage hypothesis

mutational theory

97
Q

dosage hypotheses

A

cellular oncogene directs the synthesis of an amt of normal protein product that is required for normal growth. transformation to cancerous growth results from overproduction of the normal protein.

98
Q

mutational theory

A

gene product from oncogene is different from the gene product from protooncogene.

99
Q

main classes of proto-oncogenes

A

signal transduction, cell cycle, and/or proliferation controlling molecules

100
Q

Ras

A

p21 Ras, key regulator of intracellular signaling pathways and a contributing factor in many cancers. G protein. GTPase activity.

101
Q

ligand dependent proto oncogene receptor proteins

A

Her2 and EGF receptors

102
Q

ligand independent receptor oncoproteins

A

neu and erbB

103
Q

Rb suppression results

A

one gene: no tumor
good copy inactivated: inherited mutation develop tumor
(hereditary retinoblastoma)
nonhereditary retinoblastoma: both copies of gene are inactive

104
Q

lose Rb at somatic level by

A 
deletion
point mutation
gene conversion
mitotic recombination
nondisjunction
105
Q

Li Fraumeni disease

A

one p53 allele eliminated in germ line

later somatic cell mutation causes tumor

106
Q

human papillomavirus

A

warts and cervical cancer, inactivates p53 and Rb; produces proteins E6 and E7

107
Q

arg/Pro 72

A

common polymorphism in p53. more susceptible to E6 mediated degradation. arginine form of p53 more susceptible than proline form.

108
Q

how do cancer cells preserve immortality

A

upregulate telomerase 10-20 fold

109
Q

angiogenesis activators

A

VEGF, FGFs

110
Q

angiogenesis inhibitors

A

thrombospondin, interferon a/B, angiostatin, endostatin, collagen IV fragments

111
Q

transformation of cells in culture for humans

A

telomerase, large T antigen (SV40), hits Rb and p53, Ras

112
Q

Wnt signal in gut

A

causes Wnt responsive genes to proliferate gut stem cells

113
Q

APC mutation

A

causs 80% of human colon cancer

114
Q

K-Ras and Smad4

A

also cause human colon cancer

115
Q

four genes needed for reversion of adult fibrobalstas to stem cells

A

Oct4, sox2, Kfl4, (Myc)

116
Q

Nucleotide excision repair

A

large repair, chemicals, radiation and mutages

117
Q

kartagener syndrome

A

Primary ciliary dyskinesia, also immotile ciliary syndrome or Kartagener syndrome, is a rare, ciliopathic, autosomal recessive genetic disorder that causes defects in the action of cilia lining the respiratory tract and fallopian tube, as well as in the flagella of sperm cells

118
Q

n-linked glycosylation

A

N-linked glycosylation, is the attachment of the sugar molecule oligosaccharide known as glycan to a nitrogen atom (amide nitrogen of asparagine (Asn) residue of a protein), in a process called N-glycosylation, studied in biochemistry. This type of linkage is important for both the structure and function of some eukaryotic proteins.

119
Q

O linked glycosylation

A

In the field of biochemistry, O-linked glycosylation is the attachment of a sugar molecule to an oxygen atom in an amino acid residue in a protein. O-linked glycosylation is a form of glycosylation that occurs in the Golgi apparatus in eukaryotes. It also occurs in archaea and bacteria.

120
Q

glycogenin

A

converts glucose to glycogen

Cmcb (3 decks)

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