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

CBG Lecture 10: Cell Signalling Flashcards

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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
what is the agnonist in ligand gated ion channel
nicotine
26
what is an antagonist of Nicotinic Ach receptor
curare
27
what effect does curare have on a nicotinic ACh receptor
its an antagonist
28
what are nuclear receptors
ligand modulated gene regulatory proteins that bind hydrophobic signalling molecules
29
where are nuclear receptors
cytosolic
30
what features do nuclear receptor ligands tend to have
small, hydrophobic as need to directly cross cell membran
31
give some examples of ligands for nuclear receptors
oestrogen - a steroid sex hormone retinoic acid thyroxine
32
what happens when ligand hormones bind to nuclear receptors
they bind DNA
33
outline structure of nuclear receptors
have a three part structure
34
what could be a us for steroid receptor antagonists
used in chemo for breast cancer | also tamoxifen blocks oestrogen receptors because most breast cancer cells require oestrogen to divide
35
what is estradiol
a form of oestrogen - female sex hormone
36
give an example of hormones used in chemotherapy for breast cancer
steroid receptor antagonists like tamoxifen used against breast cancer by blocking oestrogen receptors (most breast cancer cells require oestrogen to divide)
37
what are G proteins?what are they involved in
timed delayed biological switches | involved in cell signalling, im/export proteins in nucleus/vesicular traffic
38
what do G proteins bind to when active
bind to GTP
39
what is GAP
a GTPase Activating Protein
40
what is inactive form of G-protein bound to
GDP
41
what do GPCRs act as
ligand modulated GEFs
42
give an example of a GPCR
beta andrenergic receptor - adrenaline
43
outline what happens in the adrenaline cascade
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
what is CREB
cAMP response element binding protein
45
what happens in the conformational change of GPCR when adrenaline binds
alpha subunit of GPCR swaps GDP for GTP causing alpha to dissociate
46
what is the GPCR adrenaline reacts with
beta-andrenergic receptor
47
what binds to adenyl cyclase? what happens
alpha subunit binds to adenyl cyclase - convert AMP to cAMP
48
what is cAMPs target in adrenaline cascade
PKA - protein kinase A: a heterotetramer in inactive form
49
how many cAMPs does PKA need to bind to be active
4
50
what does acivated PKA do in the adrenaline cascade
phosphorylates CREB (cAMP response element brinding protein)
51
what is CREB - what does it do
cAMP response element binding protein | piece of DNA that can bind TF that starts transcrption
52
what enzyme is a G protein like
a weak GTPase
53
what are GPCRs made of - which type of receptor are they
ubiquitous 7-transmembrane receptors | they are all-trans-Retubak
54
what do GPCRs act through
second messengers
55
name some second messengers that GPCRs act through
cAMP | IP3/DAG
56
in a trimeric G protein, what does each subunit do
alpha does the work | beta and gamma can open ion channels
57
what are the characteristics of the cAMP signalling system
1. amplification 2. sharp response 3. short duration
58
what features of the cAMP signalling system show amplification
small signal leads to much cAMP
59
what features of the cAMP signalling system show sharp response
4 cAMP needed to release PKA
60
what features of the cAMP signalling system show short duration
PKA activates phosphodiesterase which rapidly removes cAMP
61
how many times do receptor tyrosine kinases pass through membrane
singlepass enzyme coupled transmembrane receptors
62
what are RTKs
receptor tyrosine kinase - ligand modulated kiases
63
what are RTKs involved in
epidermal growth factors | insulin
64
how do RTKs respond
dimerise and act through phosphorylation cascades
65
briefly describe structure of RTKs
extracellular receptor domain, transmembrane domain and intracellular tyrosine kinase domain
66
what is the extracellular receptor domain of RTK like
cysteine-rich or globulin like
67
what is the difference between RTKs and GPCRs
RTKs dont self destruct but do act as biologival switches
68
show does ligand activate RTK
cross links them and brings them close to one another
69
what do RTKs respond to
large extracellular peptides: growth factors
70
what signalling are RTKs involved in
paracrine signalling
71
what type of receptor is insuline
RTK
72
what two proteins are the main proteins involved in most growth factor cascades
RTKs and Ras
73
what is Ras
a protooncogene
74
where is Ras-GAP mutated
in neurofibromatosis
75
what happens when Ras-GEF is mutated
Ras is constituently activated -whether theres TF or not
76
how many cancers are Ras mutants
a quarter
77
how can a signal be amplified
through use of secondary messengers
78
outline steps of a generalised RTK cascade
1, ligand eg.EGF binds to EGF RTK and causes cross linking 2. mass of phosphorylation at bottom EGF RTK causes adaptor to bind a Ras-GEF protein to recognise phosphotyrosine 3. adaptor recruits GEF and Ras 4. Ras-GEF causes Ras GDP to swap out GDP for GTP 5. Ras activates MAPKKK (Raf) 6. Raf actuvates P onto MAPKK (Mek) 7. MEK adds P onto MAPK (Erk) 8. Erk phosphorylates Myc (gives 2 Ps) results in increase transcription of genes, by binding to enhancer box sequence after entering nucleus 9. Myc switches on transcription of cyclin genes
79
give an example of a ligand in RTK
epidermal growth factor
80
how do RTKs crosslink
each one of pair can phosphorylate eachother
81
what does mass of phosphorylation at bottom of EGF RTK cause
causes adaptor to bind a Ras-GEF protein to recognise phosphotyrosine
82
what does adaptor protein do
recruits GEF and Ras
83
what does RAS=GEF do
causes Ras to swap GDP for GTP
84
what is MAPKKK aka
Raf
85
what is Raf aka
MAPKKK
86
what does Raf do
activates a P onto MAPKK (MEK)
87
what is Mek
MAPKK
88
what does MAPKK do
MEK adds P onto MAPK (ERK)
89
what is ERK aka
MAPK
90
what does ERK do
phosphorylates Myc by giving it 2 Ps and results in increase transcripitoin of genes by binding to enhancer box sequence after entering nucleus
91
what does Myc do
Myc switches on transcription of cyclin genes

CBG PANT Replication, transcription and translation (10 decks)

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