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MCB II Block 1 > Cancer II 2 > Flashcards

Cancer II 2 Flashcards

1
Q

p53 can induce apoptosis in two different ways

A
  1. transcribes pro-apoptotic bcl-2 proteins

acts at mitochondrial membrane - directly binds to and 2. inhibits anti-apoptotic bcl-2 proteins

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2
Q

p53 is constantly

A

expressed in cells

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3
Q

under normal circumstances p53 is degraded by

A

MDM2

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4
Q

DNA damage what happens to p53

A

phosphorylated so MDM2 can’t bind to it

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5
Q

Mdm2 is

A

normal inhibitor of p53

so it is a proto-oncogene

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6
Q

kinase that can phosphorylate p53

A

ATM

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7
Q

ATM involved in which syndrome

A

ataxia Telangiectasia

AR

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8
Q

draw out pathway with dna damage and how p53 gets activated by it

A

43

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9
Q

p53 transcribes what to stop cell cycle

A

p21

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10
Q

if there are high levels of p53, and after cell cycle is stopped p53 levels continue to increase, what happens

A

it maks pro apoptotic

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11
Q

what does arf inhibit

A

mdm2

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12
Q

E1A

A

adenoviral oncogene that triggers excessive proliferation

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13
Q

E1A, c-myc, ras result in release of

A

release of E2F

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14
Q

E2F is involved in transcribing

A

transcribing cyclin E

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15
Q

if there are really high levels of oncogenic signaling, what happens with E2F

A

more active than usual

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16
Q

if there are really high levels of E2F it will transcribe

A

p14ARF

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17
Q

p14ARF inhibits

A

MDM2

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18
Q

ultimately what does p14ARF do

A

allows accumulation of p53 without phosphorylation

p53 doesn’t need to be phosphorylated because MDM2 is being inhibited

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19
Q

draw out cycle starting with E1A, cmyc and ras

A

pg 45

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20
Q

excessive myc production means theres a lot of

A

cyclin d being produced, ultiamtely a lto of E2F

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21
Q

MDM2 inhibits

A

p53

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22
Q

p14 arf inhibits

A

MDM2

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23
Q

p14arf indireclty allows activation of

A

p53

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24
Q

target genes for p53

A

p21
bax
dna repair enzymes

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25
Q

p53 involved in apoptosis through what method

A

transcriptional regulation

inhibits the anti-apoptotic genes

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26
Q

one of the mechanisms of apoptosis (intrinsic) is initiated by what in mitochondria

A

pore formation of outer membrane of mitochondria

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27
Q

once pore is formed in mitochonrdia what happens4

A

cytochrome c goes in and trigers apoptosis

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28
Q

bak and bax form

A

homeodoimers

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29
Q

bcl-2 is what kind of protein

A

anti-apoptotic protein

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30
Q

bak and bax are

A

pro-apoptotic proteins

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31
Q

p53 can heterodimerize with

A

bcl-2 to inhibit it - so bcl-2 can’t bind to bak or bax and therefore bak or bax will homodimerize and form pores

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32
Q

Rb is inhibitor of

A

E2F

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33
Q

p15 and p16 are

A

INK4 inhibitors of kinase 4

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34
Q

TGF beta pathway ultimately leads to increase of

A

p15 & p16

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35
Q

cyclin b cdk1 is

A

m phase cyclin

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36
Q

when is cyclin b cdk 1 expressed

A

all throughout G2 phase

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37
Q

cyclin b cdk1 is expressed through all of g2 cycle but only activated

A

when it goes from g2 into m phase

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38
Q

cyclin b cdk 1 also called

A

m cyclin

MPF

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39
Q

cyclin b is being produced all throughout

A

g2

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40
Q

cyclin b binds to

A

cdk1

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41
Q

two kinases active in regulating M-Cdk (Cyclin B CDK1)

A

wee 1

cdc25

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42
Q

cyclin b cdk 1 complex phosphorylated

A

2x

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43
Q

cdk activating kinase is

A

activating the complex cyclin b cdk 1 complex

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44
Q

wee1 kinase is

A

inactivating complex cyclin b cdk 1 complex

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45
Q

draw pathway for cyclin b cdk 1 complex in g2 phase

A

pg 54

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46
Q

when cell is ready to go into m phase there is activation of

A

cdc25

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47
Q

cdc25 is a

A

phosphatase

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48
Q

cdc25 does what

A

removes inhibitory phosphate group on cyclin b cdk 1 complex put on by wee1

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49
Q

cak stands for

A

cdk activating kinase

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50
Q

as son as cell is ready to go from g2 into m

A

cdc25 removes all the phosphates put on by wee1 on cyclin b cdk 1 complex and then it quickly goes into mitosis

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51
Q

explain how chromatin condensation, etc, stuff that is needed for mitosis is initiated

A

activated cyclin B CDK/1 complex phosphorylates the proteins associated w/ chromatin leading to condesnation of genome, etc, all the stuff needed for mitosis

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52
Q

what takes the cell through the initial phases of mitosis up to metaphase

A

cyclin B CDK-1 complex

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53
Q

chrom are maximally condensed by the time they are in

A

metaphase

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54
Q

before mitosis there is duplication of

A

centrosome

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55
Q

from two what do microtubule spindle radiate out from

A

centrosome

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56
Q

activation of m cyclin complex leads cell through

A

initial stages of mitosis up to metaphase

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57
Q

to go from metaphase to anaphase

A

there is a checkpoint

need to have activation of APC/C

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58
Q

what needs to be active to get from metaphase to anaphase

A

APC/C

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59
Q

APC/C stands for

A

anaphase-promoting complex

60
Q

ubiquitin ligases causes degradation of inhibitor of

A

separases

61
Q

separases what are they

A

enzymes that proteolytically cleave the interactions b/w sister chromatids

62
Q

separases function

A

separate sister chromatid allowing them to be pulled apart to separate poles

63
Q

without metaphse to anaphse checkpoint could end up with

A

aneuploidy

64
Q

mad2 function

A

sense if all sister chromatids are boudn to microtubule spindle
if they aren’t lined up prevents apc/c so it doesn’t go into anaphse until its ready

65
Q

mad 2 prevents activation of

A

apc/c

66
Q

telophase

A

nuclear envelope reforms

67
Q

in metaphase there is degradation of what and then activation of what

A

degradation of all the cyclin CDK complexes, activation of APC/C

68
Q

activation of APC/C allows cell to go from

A

metaphase to anaphase

69
Q

is there inflammation with apopt.

A

no

70
Q

when cells are apoptotic they split into

A

apoptotic bodies

71
Q

when cell is apoptotic what is flipped

A

phosphotidyl serine is flipped to outer leaflet, “eat me” to macrophages

72
Q

necrosis vs apoptosis

A

necrosis has inflammation

73
Q

when is apoptosis important in development

A

limb formation, dies so we get fingers, etc.

hollow structures

74
Q

describe some things that happen to the cell during apoptosis

A

Phosphatidylserine translocated from cytoplasmic leaflet to extracellular leaflet of plasma membrane
Membrane “blebbing”: Cell contents not released, little inflammation
Loss of substrate attachment, rounded phenotype
Decrease in cell volume
Depolarization of mitochondrial membrane potential
Activation of caspases (cysteine proteases),
Endonuclease activation DNA degradation, RNA also degraded
Chromatin condensation forming crescent bodies

75
Q

annexin

A

binds to phosphotidyl serine so you can see cells that are apoptotic
used in labs

76
Q

two apoptotic pathway

A

intrinsic (mitochondrial pathwya)

extrinisic pathway

77
Q

death receptor function as

A

trimers

78
Q

DR stands for

A

death receptor

79
Q

FAS and TNFR1 are

A

death receptors

80
Q

death receptors all have

A

death domain

81
Q

death receptors all function as

A

trimers

82
Q

when signaling molecule from outside binds to death receptors it causes

A

FADD binds to receptor which recruits pro-caspase-8 which results in cleavage of pro-caspase 8 into caspase 8

83
Q

FADD

A

fast associated death domain protein

84
Q

what is major caspase of extrinsic pathway

A

caspase 8

85
Q

caspase cascade

A

when one pro-caspase cleaved and activated it will go cleave and activate another caspase

86
Q

caspases are present in cell as

A

pro-caspases (inactive)

87
Q

one pro-caspases needs to do what to get active

A

cleaved

88
Q

caspase 8 will do what

A

cleave and activate effector capases (3, 6, 7) and those will digest the cell

89
Q

caspase 3 6 and 7 do what

A

digest the cell

90
Q

draw out extrinsic receptor mediated pathway

A

pg 76

91
Q

caspase 3, 6, and 7 are also known as

A

executioner caspases

92
Q

caspases 3 6 and 7 also cleave the ihibitor of an

A

endonuclease (endoncleases are activated to start digesting the genome)

93
Q

DISC stands for

A

death inducing signaling complex

94
Q

formation of disc activates

A

pro-caspase 8

95
Q

intrinsic apoptotic pathway is also known as

A

mitochonrdial pathway

96
Q

what initiates the intrinsic pathway

A

pore formation in outer membrane of mitochondria

97
Q

what is initiater caspase for intrinsic pathway

A

pro-caspase 9

98
Q

cytochrom c binds to

A

apaf-1

99
Q

binding of cytochrome c to apaf-1 forms what complex

A

apoptosome

100
Q

apoptosome activates

A

caspase 9

101
Q

caspase 9 will

A

cleave and activate effector caspase 3, 6, 7

102
Q

extrinsic and intrinsic pathway are identical once

A

effector caspases are active

103
Q

caspase 3, 6, 7 cleave

A

proteins w/in cell, everything gets digested incell

104
Q

IAP stand for

A

inhibitors of apoptosis

105
Q

IAP inhibit

A

executioner caspases

106
Q

IAP what happens in cancer

A

over expressed - b/c they inhibit apopt.

107
Q

smac/diablo protein inhibits

A

the inhibitors of apoptosis IAP

108
Q

smac/diablo is

A

tumor supressor - promotes apoptosis by inhibitong inhibitors of apoptosis

109
Q

apoptotic stimulus

A

pro formation in outer membrane of mitocrhondria

110
Q

caspase 3 when activated

A

cleave the inhibitor of endonuclease

111
Q

endonuclease activity with activation of

A

caspase 3

112
Q

endonuclease will start

A

digesting genome

113
Q

cell that is apoptotic will see what regarding dna

A

dna ladder

114
Q

bcl-2 includes

A

pro-apoptotic and antiapoptoci

115
Q

antiapoptic bcl-2 proteins

A

Bcl-2 and bcl-xl

116
Q

pro-apoptotic bcl-2 proteins

A

bax, bad, bak, bid

117
Q

anti-apoptotic genes are type of

A

oncogene

118
Q

bax and bak direclty form

A

pores in outer membrane in mitochondria

119
Q

bcl-2 and bcl-xl inhibit

A

bak and bax

120
Q

bad and bid inhibit

A

bcl-2 and bcl-xl

121
Q

in order to get pore formation in mitochondria need

A

bak or bax homodimerization

122
Q

bcl-2 can heterodimerize with

this does what

A

bak or bax

prevents them from forming pores

123
Q

bak and what do same thing

A

bax

124
Q

bad and bid form heterodiers with

this does what

A

bcl-2 or bcl-xl

allows pore formation

125
Q

pore formation result in release of

A

cytochrome c

126
Q

caspase 8 also cleaves (beside executioner)

A

BID

127
Q

BID when cleaved, releases

A

TBID

128
Q

TBID stands for

A

truncated BID

129
Q

TBID can heterodimerize with

A

bcl-2 or bcl-xl

130
Q

TBID is

A

pro-apoptotic bcl-2 protein that gets activated following extrinsic pathway but stimulates intrinsic pathway

131
Q

when there is dna damage what pathway will be activated

A

intrinsic apoptotic

132
Q

smac mimetic

A

mimics what smac does

drugs target cancer with overexpression of iap - they bind and inhibit iap

133
Q

mimetic

A

drug that mimics

134
Q

p53 promotes transcription of what pro-apoptotic proetins

A

bac and bax

135
Q

p53 can heterodimerize with

A

bcl-2 bcl-xl

136
Q

what other protein can bind and heterodimerize with bcl-2 and bcl-xl

A

TBID p53 bad

137
Q

bcl-2 inhibits

A

bax

138
Q

when p53 is around what does it do regarding bcl-xl

A

binds to bcl-xl so bax is free and can cause pore formation

139
Q

draw pathway for p53 and the intrinsic pathway

A

pg 94

140
Q

draw pi3k and akt, pten pathway

A

pg 97 98 99

141
Q

is p14 arft a proto-oncogene or tumor suppressor gene

A

tumor suppressor gene - it’s allowing accumulation of p53 through inhibiting its inhibit mdm2

142
Q

what makes arf

A

E2F

143
Q

pore formation is induced by what genes

A

pro-apoptotic bcl-2 genes

144
Q

What are the two HPV oncoproteins

A

E6 & E7

145
Q

How does HPV oncoprotein E6 cause cancer

A

degrades p53

146
Q

How does HPV oncoprotein E7 cause cancer

A

binds & inhibits Rb

MCB II Block 1 (12 decks)

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