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CAN > L04: Cell Signalling And Cancer > Flashcards

L04: Cell Signalling And Cancer Flashcards

1
Q

What is intracellular signalling

A

A set of events that occur inside a cell to a specific stimulus with a specific cellular response

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2
Q

What events does cell signalling allow

A

Survival
Proliferation
Differentiation
Apoptosis

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3
Q

What are the signalling molecules that can trigger a intracellular response

A

Hormone
Cytokines
Growth factors
Neurotranmistters

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4
Q

What type of molecule binds to intracellular receptors

A

Hydrophobic

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5
Q

What type of molecules binds to cell surface receptors

A

Hydrophilic

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6
Q

Name an important cell surface receptor family

A

Receptor tyrosine kinases

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7
Q

Where are receptor tyrosine kinases bound to

A

Single plasma membrane

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8
Q

How many domains does receptor tyrosine kinase have

A

Intracellular domain

Extracellular domain

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9
Q

Where is the intracellular domain found

A

Within the cytoplasm behind the plasma membrane

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10
Q

Where is the extracellular domain found

A

Outside the plasma membrane

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11
Q

For all receptor tyrosine kinases which domain is the same

A

Intracellular domain

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12
Q

What is the intracellular domain of the receptor tyrosine kinase made of

A

Tyrosine kinase domains

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13
Q

What is the role of tyrosine kinase domain

A

Phosphorylate target proteins

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14
Q

Which domain of the receptor tyrosine kinase vary

A

Extracellular domain

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15
Q

If the extracellular domain of receptor tyrosine kinase vary what does this mean

A

Different proteins can bind to it

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16
Q

What are the 2 types of tyrosine kinase receptor transduction signalling pathway when signalling molecules interact with TPR

A

1) mitogen activated protein (MAP) pathway

2) phosoptidylinositol (pi)-3 kinase pathway

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17
Q

What is the main output of the MAP kinase pathway

A 
Cell growth (cell getting bigger)
Cell profileration (cell dividing in numbers)
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18
Q

What happens to the TPR when a signalling molecule binds to it

A

Dimerisation of receptor

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19
Q

What happens when receptor dimerisation occurs

A

Kinase domains of neighbouring receptors cross phosphorylate eachother on multiple tyrosine residues

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20
Q

What is the phosphorylation of neighbouring receptors on tyrosine residues known as

A

Auto phosphorylation

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21
Q

What does autophosrylation creature

A

High affinity for:
MAP pathway
PI-3 kinase pathway

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22
Q

Which molecule for the MAP pathway recognises the phosphorylated tyrosine residues in TPR

A

Grb-2

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23
Q

What are the 2 domain of Grb-2

A

SH2 domain

SH3 domain

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24
Q

Which domain of grb-2 binds to the phosphorylated tyrosine resides

A

SH2 domain

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25
Q

What does the SH3 domain of the Grb-2 bind to

A

Protein called sos

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26
Q

What does the grb-2 and sos complex enable

A

SOS to recruite and acitvate RAS

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27
Q

What is RAS

A

A G protein with GTPase activity

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28
Q

What is ras known as in cancer

A

Oncogene

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29
Q

Where is ras attached to

A

The plasma membrane next to the TPR

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30
Q

How does sos active RAS

A

SOS exchanges GDP (found in inactive ras) to GTP to activate ras

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31
Q

What does active ras do

A

Activates RAF by inducing a conformation change to it

32
Q

When RAF is activated what does it do

A

Activates Mek by phosphorylating it

33
Q

What does active mek do

A

Active Erk by phosphorylation

34
Q

What does ERK do

A

Moves into the nucleus and phosphorylates proteins that include gene regulatory proteins that cause change in gene expression

35
Q

What are the genes active by Erk

A 
C-jun
C-fas
C-MYC 
C-MYC 
Cyclin D
36
Q

What does ERK overall do

A

Cell proliferation and cell growth

37
Q

In normal conditions how is MAP kinase regulated

A

Switching acitvated TPR
Inactivating ras
Inactivate target proteins

38
Q

How is activated TPR switched off

A

By a protein protein tyrosine phosphotases

39
Q

How is active ras inactivated

A

Via ras GAPS

40
Q

How are target proteins inactivated

A

De phosphorylation by serine/threonine phosphatase

41
Q

What can happen for cancer to develop due to MAP pathway

A

Proteins can become permanent turned on

42
Q

What are the main outputs of PI-3kinase pathway

A

Cell survival

Cell growth/proliferation

43
Q

Which molecule of the PI-3 kinase pathway recognises the phosphorylated tyrosine residues on RTK

A

PI-3 kinase

44
Q

When PI-3 kinase binds to tyrosine residues what does it do

A

Become activated

45
Q

What does acitvated PI-3 kinase do

A

Phosphorylate PI(4,5)P2 TO (PI,3,4,5)P3

46
Q

Where is PI(4,5)P2 found

A

Attached to plasma membrane next to the RTK

47
Q

What happens when we have PI(3,4,5) P3

A

PDK1 and AKT proteins bind to it

48
Q

Which molecule binds to PI(3,4,5)P3 first

A

PDK1

49
Q

When PDK1 binds what happens to AKT that is also bound to another PI(3,4,5)P2

A

PI(3,4,5)P3 that had PDK1 bound to acitvates AKT by phosphorylating it

50
Q

What other molecule is AKT phosphorylated by

A

MTOR

51
Q

As a result of phosphorylating AKT what happens to it

A

It becomes active

52
Q

What does active AKT DO

A

Phosphorylate Bad

53
Q

What is the bad

A

A protein that bind to inactive apoptosis inhibitory protein

54
Q

What happens when active AKT phosphorylates BAD

A

Acitve apotosis inhibitory protein becomes released from bad and this prevents apoptosis i.e promote cell survival

55
Q

How is PI-3 kinase pathway regulated

A

Switch TKP
De phosphorylate target proteins
Remove phosphate from PI(3,4,5)P3

56
Q

How it active TKP swithched off

A

Protein tyrosine phosphatase

57
Q

How is target proteins de phosphorylated

A

Serine/threonine phosphatase

58
Q

What removes the phosphate from PI(3,4,5)P3

A

PTEN

59
Q

If the MAP and PI-3 kinase pathway is disrupted what can this lead to

A

Cell proliferation and cancer

60
Q

How can we treat people with cancer that have disrupted pathways of MAP or PI-kinase pathway

A

Personalised medicine

61
Q

What is HER2

A

Member of EGFR family (type of receptor tyrosine kinase)

62
Q

How does HERF2 usually work

A

Heterodimerise with another EGFR receptor in repsonse to the signalling molecule of EGF to activate the PI3 Kinase and MAP pathway

63
Q

What does dimerisation of EGFR lead to

A

Activation of MAP and PI-3 kinase pathway for cell survival and cell growth

64
Q

In cancer what can happen to HER2

A

Become over expressed

65
Q

Which type of cancer shows overexpression of HER2

A

Breast cancer

66
Q

In cancer with overexpression of HER2 what happens

A

Homodimerisation of HER2 (i.e phosphorylation of 2 HER2) which triggers cell growth and survival in the absence of EGF

67
Q

What personalised medicine can be used to prevent HER2 overexpression

A

Herceptin

68
Q

What does herceptin cause

A

HER2 degradation

Antibody dependent cellular cytotoxicity (APCC) response

69
Q

What patients can herceptin be used on

A

HER2 positive patients (not in HER2 normal patients)

70
Q

What is BRC-ABL

A

Oncogenic protein

71
Q

How is BCR-ABL formed

A

Translocation of chromosome 22 and 9

72
Q

Which cancer is BCR-ABL seen in

A

CML: chronic myelogenous

73
Q

In a normal cell what is ABL

A

A tyrosine kinase protein that promotes cell survival and growth by dimerising tyrosine residues on RTK and activate MAP and PI3 kinase

74
Q

What happens when BCR joins to ABL to form BCR-ABL

A

It promotes acitvation of ABL which goes onto dimerise tyrosine residues on RTK

75
Q

What type of personalised medicine can be used to target BCR-ABL

A

Imatinib

76
Q

What is the role of imatinib

A

Binds to kinase domain of ABL to prevent ATP binding cannot phosphorylate itself to cause downstream signalling

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