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Cell biology semester 1 > cell signalling > Flashcards

cell signalling Flashcards

1
Q

components of cell signalling pathway

A

signal
reception
transduction
amplification
response

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2
Q

how to alter activity of proteins in a signalling pathway?

A

changing level of protein
changing activity of fixed amount of protein

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3
Q

how do you change the activity of a fixed amount of protein fast?

A

covalent modification
conformational change

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4
Q

percentage of genome of eukaryotic cells coding for signalling molecules

A

10-15%

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5
Q

gap junctions

A

allows small signaling molecules to pass directly from cell-to-cell
e.g. ions/ metabolites (NOT macromolecules)

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6
Q

contact-dependent

A

signalling molecule on cell surface interacts directly with receptor on recipient cell
important for immune signalling development

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7
Q

paracrine signalling

A

acts on different cell types in close proximity
important in development and inflammation

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8
Q

autocrine signalling

A

self signalling
other cells of same type can also bind

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9
Q

types of signaling from local to distant

A

gap junction
contact-dependent
autocrine
paracrine
synaptic
endocrine

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10
Q

intracellular reception

A

small hydrophilic signalling molecules can cross membrane and bind to intracellular receptors
e.g. steroid hormones/ NO gas

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11
Q

cell-surface receptors

A

hydrophilic signaling molecules

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12
Q

nuclear hormone receptors

A

conformational change in response to ligand-binding
receptor-ligand complex regulates transcription of target genes

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13
Q

androgen receptors

A

androgen steroids determine male secondary sexual characteristics
no androgen signalling = female development

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14
Q

androgen insensitivity syndrome

A

deficiency of androgen receptors
male embryo produces normal testosterone not detected by target cells
therefore genetically male but phenotypically female

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15
Q

nitric oxide receptors

A

conformational change in response to ligand-binding
produces secondary messenger cGMP

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16
Q

3 types of cell surface receptor

A

ion channel coupled
G-protein coupled
enzyme coupled

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17
Q

ion channel coupled receptors

A

alters membrane permeability to ions
converts chemical signal to electrical in nerve synapses

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18
Q

myasthenia gravis

A

rare autoimmune disorder involving antibody build up on nicotinic ACh receptors
symptoms: drooping eyelids, movement difficulty

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19
Q

G-protein coupled/ serpentine receptors

A

largest family of CS receptors
7 pass transmembrane proteins
mediated by trimeric G-proteins

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20
Q

2 types of G-protein

A

trimeric (transduce signals from G-protein coupled receptors)
monomeric (transduce signals from enzyme-coupled receptors)

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21
Q

what do G proteins bind?

A

GDP or GTP
guanosine di/tri phosphate

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22
Q

trimeric G proteins

A

transduce at G protein coupled receptors
3 heterologous sub-units

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23
Q

alpha sub-unit of trimeric G-protein

A

has intrinsic GTPase activity
binds GDP in resting state

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24
Q

consequence of signal binding on trimeric G-protein

A

conformational change in receptor/ alpha sub-unit
a subunit releases GDP and binds GTP
activated a, b and gamma subunits dissociate

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25
how do G-proteins turn themselves off?
GTP-hydrolysis into GDP/ dihydrogen phosphate
26
2 enzymes involved in G protein activation of downstream signaling pathways
adenlyl cyclase phospholipase C
27
adenlyl cyclase conversion
ATP> cAMP
28
phospholipase C breakdown
inositol 1,4,5-triphosphate and diacylglycerol
29
how does cAMP pass down info?
via cAMP-dependent protein kinase PKA cAMP binds to PKA, inducing conformational change, releasing and activating catalytic sub-units which pass down info via phosphorylation of other proteins
30
why are epinephrine signals amplified
to ensure fast response
31
phospholipase action
cleaves phosphoinositol 4,5biphosphate to produce IP3 and DAG
32
IP3 action
releases Ca2+ from ER
33
DAG action
activates protein kinase C cooperates w Ca2+ to activate PKC
34
cytosolic Ca2+ levels
10^-7M low therefore small changes easily detected
35
extracellular Ca2+ levels
10^-3M
36
calmodulin
mediates Ca2+ dependent effects each binds 4Ca2+ conformational change allows calmodulin/Ca2+ complex to wrap tightly around target protein
37
enzyme-linked receptors
single span transmembrane cytosolic domain has intrinsic enzymatic activity/ associated w enzyme
38
RTK
Receptor tyrosine kinases common enzyme-linked receptor cytoplasmic domain has intrinsic kinase activity
39
RTK examples
growth factor receptors (cell proliferation control) insulin receptors (tetramers, binding causes realignment of polypeptide chains, activating cross-phosphorylation)
40
binding of ligand to growth factor receptor
cross-linking of 2 receptor chains
41
oligomerisation of receptor chains
allows cross/auto phosphorylation
42
phosphorylated tyrosine residues
provide docking sites for other signalling proteins
43
RAS
small monomeric G-protein/ proto-oncogene main signal transducer protein for growth factors activates downstream phosphorylation cascade for map kinase pathway
44
% RAS mutations of cancers % pancreatic
20-30% of cancers 80% pancreatic
45
difference between trimeric and monomeric G-proteins
t binds directly to receptor/ m indirect t activates GDP release/ m requires GEF to activate GDP release t GTP hydrolysis via intrinsic GTPase activity alone/ m requires GAP
46
GEF
Guanine nucleotide exchange factor
47
GAP
GTPase activating protein
48
RAS and GEF binding to RTK
mediated by Grb-2 adapter protein
49
RAS mutation
affects GTP hydrolysis activity GTP stays bound longer and signaling pathway continuously switched on therefore cell proliferation occurs in absence of growth factors
50
how can cells respond differently to the same signal
via different receptors different intracellular machinery activation
51
nicotinic ACh receptor
ion channel linked/ inotropic and fast membrane depolarisation induces skeletal muscle contraction
52
muscarinic ACh receptor
G-protein linked/ metabotropic and slow hyperpolarisation of membrane reduces rate of contraction of heart muscle
53
nitric oxide receptors
conformational change produces c GMP as secondary messenger
54
crosstalk
overlap between many different signalling pathways
55
cross talk pro and con
:) allows fine-tuning of response :( risk of producing wrong response
56
types of crosstalk
additive (1+1=2) synergism (1+1>2) antagonism (1+1<2)
57
3 types of signalling complexes
stable (components linked by scaffold protein) transient (signalling complex assembles after receptor activated) transient (modification of plasma phospholipid molecules)
58
how to switch off signal
removal/ inactivation of signal/ receptor inactivation of activated signal proteins degradation of 2nd messengers
59
removal of cell signal
degradation recycling sequestration
60
what does rate of signal removal affect
response duration
61
receptor removal
allows cell desensitization involves ligand-dependent receptor-mediated endocytosis
62
inactivation of activated proteins
GTP hydrolysis dephosphorylation/ phosphorylation
63
cholera toxin
interferes w G-protein hydrolysis ADP-ribosylation of G-alpha prevents GTP hydrolysis and therefore locks G protein in active state ^cAMP so Cl- and water lost to intestinal lumen
64
allosteric inactivation
dissociation from activator/ association w inhibitor
65
removal of secondary messengers catalysis
phosphodiesterase
66
viagra
inhibits cGMP phosphodiesterase so ^cGMP and prolonged muscle relaxation competitive inhibitor

Cell biology semester 1 (6 decks)

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