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CBG PANT Replication, transcription and translation > CBG Lecture 10: Cell Signalling > Flashcards

CBG Lecture 10: Cell Signalling Flashcards

1
Q

what happens if there are holes in a membrane

A

cell tends towards thermodynamic equbm, resting potential dissipates (0mV) creates action potential

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2
Q

give an example of a signal that indicates death

A

oxidised fat leakage - nearby cells recognise it and activate their defences

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3
Q

give generalised flowchart of cell signalling

A

signal (ligand) - receptir (transmembrane/cytosolic) - cascade (sometimes, amplification,switches) - gene expression (TFs) - enzyme activity

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4
Q

what 4 ways of signalling are

A

juxtacrine
autocrine
paracrine
endocrine

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5
Q

which types of cell signalling are short disctance

A

autocrine

juxtacrine

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6
Q

which types of cell signalling are long distance

A

endocrine

paracrine

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7
Q

what is juxtacrine signalling

A

cell directly interacts with other cell via membrane bound ligands

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8
Q

give an example of juxtacrine signalling

A

Th cell stimulation of B cell,
gap junctions
plasmodesmata

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9
Q

which type of signalling requires direct contact with other cell

A

juxtacrine

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10
Q

what is autocrine signalling

A

self stimulation

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11
Q

give an example of autocrine signalling

A

selinterleukin 2 from a stimulated T cell causes that T cell to proliferate monoclonally

positive feedback loop

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12
Q

what type of signalling is self stimulation

A

autocrine

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13
Q

what is paracrine signalling

A

signalling to other nearby cells

local cells

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14
Q

which type of signalling is done to nearby cells

A

paracrine

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15
Q

give an example of paracrine signalling

A

neuronal signalling

many growth factors

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16
Q

what is endocrine signalling

A

distant cells secrete signalling molecules into transport systems

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17
Q

what is the longest distance cell signalling

A

endocrine

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18
Q

give an example of endocrine signalling

A

insulin via blood in mammals

gibberellin via xylem in plants

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19
Q

give an example of when the same ligand has different effects on different cells

A

ACh on…..
1. heart muscle: decreased contraction

  1. Salivary glands: secretory enzymes
  2. Skeletal muscle: contraction
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20
Q

how does ACh have different effects?

A

different cells/different receptors

eg. heart/salivary glands/skeletal muscles

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21
Q

what is an agonist

A

opens the ligand gated ion channel

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22
Q

what is an antagonist

A

closes the ligand gated ion channels by blocking them : paralysis

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23
Q

what are the main classes of cell signalling receptors

A
  1. nuclear receptor
  2. Gprotein coupled receptor
  3. enzyme coupled receptor
  4. ligand gated ion channels
  5. adhesion receptors
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24
Q

give an example of a ligand gated ion channel

A

nicotinic ACh receptor is a ligand gated Na+ channel : musculoskeletal junctions. CNS synapses

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25
Q

what is the agnonist in ligand gated ion channel

A

nicotine

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26
Q

what is an antagonist of Nicotinic Ach receptor

A

curare

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27
Q

what effect does curare have on a nicotinic ACh receptor

A

its an antagonist

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28
Q

what are nuclear receptors

A

ligand modulated gene regulatory proteins that bind hydrophobic signalling molecules

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29
Q

where are nuclear receptors

A

cytosolic

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30
Q

what features do nuclear receptor ligands tend to have

A

small, hydrophobic as need to directly cross cell membran

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31
Q

give some examples of ligands for nuclear receptors

A

oestrogen - a steroid sex hormone
retinoic acid
thyroxine

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32
Q

what happens when ligand hormones bind to nuclear receptors

A

they bind DNA

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33
Q

outline structure of nuclear receptors

A

have a three part structure

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34
Q

what could be a us for steroid receptor antagonists

A

used in chemo for breast cancer

also tamoxifen blocks oestrogen receptors because most breast cancer cells require oestrogen to divide

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35
Q

what is estradiol

A

a form of oestrogen - female sex hormone

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36
Q

give an example of hormones used in chemotherapy for breast cancer

A

steroid receptor antagonists like tamoxifen used against breast cancer by blocking oestrogen receptors (most breast cancer cells require oestrogen to divide)

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37
Q

what are G proteins?what are they involved in

A

timed delayed biological switches

involved in cell signalling, im/export proteins in nucleus/vesicular traffic

38
Q

what do G proteins bind to when active

A

bind to GTP

39
Q

what is GAP

A

a GTPase Activating Protein

40
Q

what is inactive form of G-protein bound to

A

GDP

41
Q

what do GPCRs act as

A

ligand modulated GEFs

42
Q

give an example of a GPCR

A

beta andrenergic receptor - adrenaline

43
Q

outline what happens in the adrenaline cascade

A

adrenaline interacts with the beta andrenergic receptor which is a GPCR
conformational change, alpha unit of GPCR swaps GDP for GTP and causes alpha unit to dissociate
alpha unit then binds to adenyl cyclase, interacts with eachother and converts ATP to cAMP
flood cell with cAMP: amplificaiton
cAMPs target is PKA (protein kinase A) a heterotetramer in inactive form
when PKA binds 4xcAMP, releases active form of PKA
Activated PKA phosphorylates CREB - TF can enter nucleolus and bind to cAMP response element = start transcription

44
Q

what is CREB

A

cAMP response element binding protein

45
Q

what happens in the conformational change of GPCR when adrenaline binds

A

alpha subunit of GPCR swaps GDP for GTP causing alpha to dissociate

46
Q

what is the GPCR adrenaline reacts with

A

beta-andrenergic receptor

47
Q

what binds to adenyl cyclase? what happens

A

alpha subunit binds to adenyl cyclase - convert AMP to cAMP

48
Q

what is cAMPs target in adrenaline cascade

A

PKA - protein kinase A: a heterotetramer in inactive form

49
Q

how many cAMPs does PKA need to bind to be active

A

4

50
Q

what does acivated PKA do in the adrenaline cascade

A

phosphorylates CREB (cAMP response element brinding protein)

51
Q

what is CREB - what does it do

A

cAMP response element binding protein

piece of DNA that can bind TF that starts transcrption

52
Q

what enzyme is a G protein like

A

a weak GTPase

53
Q

what are GPCRs made of - which type of receptor are they

A

ubiquitous 7-transmembrane receptors

they are all-trans-Retubak

54
Q

what do GPCRs act through

A

second messengers

55
Q

name some second messengers that GPCRs act through

A

cAMP

IP3/DAG

56
Q

in a trimeric G protein, what does each subunit do

A

alpha does the work

beta and gamma can open ion channels

57
Q

what are the characteristics of the cAMP signalling system

A
  1. amplification
  2. sharp response
  3. short duration
58
Q

what features of the cAMP signalling system show amplification

A

small signal leads to much cAMP

59
Q

what features of the cAMP signalling system show sharp response

A

4 cAMP needed to release PKA

60
Q

what features of the cAMP signalling system show short duration

A

PKA activates phosphodiesterase which rapidly removes cAMP

61
Q

how many times do receptor tyrosine kinases pass through membrane

A

singlepass enzyme coupled transmembrane receptors

62
Q

what are RTKs

A

receptor tyrosine kinase - ligand modulated kiases

63
Q

what are RTKs involved in

A

epidermal growth factors

insulin

64
Q

how do RTKs respond

A

dimerise and act through phosphorylation cascades

65
Q

briefly describe structure of RTKs

A

extracellular receptor domain, transmembrane domain and intracellular tyrosine kinase domain

66
Q

what is the extracellular receptor domain of RTK like

A

cysteine-rich or globulin like

67
Q

what is the difference between RTKs and GPCRs

A

RTKs dont self destruct but do act as biologival switches

68
Q

show does ligand activate RTK

A

cross links them and brings them close to one another

69
Q

what do RTKs respond to

A

large extracellular peptides: growth factors

70
Q

what signalling are RTKs involved in

A

paracrine signalling

71
Q

what type of receptor is insuline

A

RTK

72
Q

what two proteins are the main proteins involved in most growth factor cascades

A

RTKs and Ras

73
Q

what is Ras

A

a protooncogene

74
Q

where is Ras-GAP mutated

A

in neurofibromatosis

75
Q

what happens when Ras-GEF is mutated

A

Ras is constituently activated -whether theres TF or not

76
Q

how many cancers are Ras mutants

A

a quarter

77
Q

how can a signal be amplified

A

through use of secondary messengers

78
Q

outline steps of a generalised RTK cascade

A

1, ligand eg.EGF binds to EGF RTK and causes cross linking

  1. mass of phosphorylation at bottom EGF RTK causes adaptor to bind a Ras-GEF protein to recognise phosphotyrosine
  2. adaptor recruits GEF and Ras
  3. Ras-GEF causes Ras GDP to swap out GDP for GTP
  4. Ras activates MAPKKK (Raf)
  5. Raf actuvates P onto MAPKK (Mek)
  6. MEK adds P onto MAPK (Erk)
  7. Erk phosphorylates Myc (gives 2 Ps) results in increase transcription of genes, by binding to enhancer box sequence after entering nucleus
  8. Myc switches on transcription of cyclin genes
79
Q

give an example of a ligand in RTK

A

epidermal growth factor

80
Q

how do RTKs crosslink

A

each one of pair can phosphorylate eachother

81
Q

what does mass of phosphorylation at bottom of EGF RTK cause

A

causes adaptor to bind a Ras-GEF protein to recognise phosphotyrosine

82
Q

what does adaptor protein do

A

recruits GEF and Ras

83
Q

what does RAS=GEF do

A

causes Ras to swap GDP for GTP

84
Q

what is MAPKKK aka

A

Raf

85
Q

what is Raf aka

A

MAPKKK

86
Q

what does Raf do

A

activates a P onto MAPKK (MEK)

87
Q

what is Mek

A

MAPKK

88
Q

what does MAPKK do

A

MEK adds P onto MAPK (ERK)

89
Q

what is ERK aka

A

MAPK

90
Q

what does ERK do

A

phosphorylates Myc by giving it 2 Ps and results in increase transcripitoin of genes by binding to enhancer box sequence after entering nucleus

91
Q

what does Myc do

A

Myc switches on transcription of cyclin genes

CBG PANT Replication, transcription and translation (10 decks)

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