T2- TSG's Flashcards

1
Q

RB binds to and inactivates

A

E2F

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2
Q

E2F can dimerize with DP and activates __

A

transcription

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3
Q

RB is a major on/off switch for the

A

G1–> S checkpoint

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4
Q

what happens if a person only have 1 functional gene for RB

A

can go through checkpoint much faster and more likely to develop retinoblastoma

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5
Q

CDK inhibitors mainly work by

A

binding the CDK so that it can’t be phosphorylated.

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6
Q

what is p53

A

a tumor supressor gene that is a DNA binding protein that regulates the transcription of several other genes.

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7
Q

p53 increases expression of__

A

p21 (CDK inhibitor) and GADD45 (growth arrest and DNA damage–promotes repair)

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8
Q

if DNA repair is not successful

A

p53 activates production of apoptosis–inducing BAX

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9
Q

if DNA repair is successful

A

p53 activates production of MDM2, which promotes degradation of p53 since its job is done.

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10
Q

syndrome in which the person is only born with 1 functional p53 allele.

A

Li-Fraumeni syndrome (LFS)

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11
Q

what activates p53

A

it has to be phosphorylates

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12
Q

name and describe the 3 kinases that activate p53

A
  1. ATM (ataxia telangiectasia mutated)–> respond to sensors when sDNA breaks and stops cell cycle to allow for DNA repair
  2. ATR–> respond to ssDNA damage
  3. Chk1 and Chk2–> ser/thr kinases that are activated by ATM and ATR kinases to respond to DNA damage.
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13
Q

if p53 is NOT phosphorylated it is bound to mdm2:

A

an E3 ubiquitin-protein ligase and important negative regulator of p53.
-USP7 removes ubiquitin groups form p53, thus stabilizing and promoting p53 activity.

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14
Q

WNT ligands bind to the ___ receptor. WNT signals are _____ signals

A

WNT. pro growth signals

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15
Q

Pitt Hopkins syndrome mutation

A

no TCF. no transcription inhibitors.

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16
Q

3 isoforms of TGF-beta

A

B1, B2, B3

17
Q

TGF-beta mediates

A

an anti growth signal. activates a cascade of 2nd messengers –> the SMADS

18
Q

SMADs

A
  1. r-SMAD–> receptor stimulated
  2. I-SMAD–> inhibitory
  3. Co-SMAD–> SMAD4
19
Q

For SMAD to bind to DNA and promote transcription it has to

A

dimerize with SMAD4

20
Q

purpose of SMURF

A

ubiquinates SMAD which promotes degradation.

21
Q

if you overexposes smurfs, you kill

A

all the SMADs and their won’t be any anti-growth signals= cancer.

22
Q

NF-1

A

gene that is mutated codes for GAP

23
Q

if you have a mutated GAP

A

then Ras will stay active much longer.

24
Q

NF-2

A

MERLIN gene–> coding coordinates membrane receptor signaling and cell:cell contact

25
Q

NF-2 deficiency results in developing of

A

benign bilateral schwannomas of the vestibular nerve

26
Q

VHL is a protein that is

A

missing a ubiquitin ligase and promotes degradation of HIF1alpha

27
Q

loss of VHL–>

A

increased HIF1alpha activity–> increased angiogenic growth factor synthesis.

28
Q

PTEN pathway

A

2nd messenger system:
-binding of ligand to membrane receptors activates PI3K.
Activated PI3K phosphorylates PIP2 to produce PIP3.
- PIP3 recruits PDK1 to the plasma membrane: PDK1 phosphorylates and activates AKT
-PTEN dephosphorylates PIP3.

29
Q

cowden syndrome is a mutation of the

A

PTEN. characterized by multiple tumor like growths

30
Q

E-cadherin acts as an

A

invasion suppressor.

31
Q

KLF6 is

A

an important TSG, mutated in 75% of prostate cancer. increases transcription of p21 and TGF-beta receptors.

32
Q

G2/M checkpoint ensures

A

that DNA damage that occurs during/after replication is repaired before cell enters mitosis.

33
Q

mutated CDC25

A

unable to be phosphorylated by CHK1–> no G2 arrest.