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Cell biology semester 1 > cell signalling > Flashcards

cell signalling Flashcards

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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
Q

how do G-proteins turn themselves off?

A

GTP-hydrolysis into GDP/ dihydrogen phosphate

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26
Q

2 enzymes involved in G protein activation of downstream signaling pathways

A

adenlyl cyclase
phospholipase C

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27
Q

adenlyl cyclase conversion

A

ATP> cAMP

28
Q

phospholipase C breakdown

A

inositol 1,4,5-triphosphate and diacylglycerol

29
Q

how does cAMP pass down info?

A

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
Q

why are epinephrine signals amplified

A

to ensure fast response

31
Q

phospholipase action

A

cleaves phosphoinositol 4,5biphosphate to produce IP3 and DAG

32
Q

IP3 action

A

releases Ca2+ from ER

33
Q

DAG action

A

activates protein kinase C
cooperates w Ca2+ to activate PKC

34
Q

cytosolic Ca2+ levels

A

10^-7M
low therefore small changes easily detected

35
Q

extracellular Ca2+ levels

A

10^-3M

36
Q

calmodulin

A

mediates Ca2+ dependent effects
each binds 4Ca2+
conformational change allows calmodulin/Ca2+ complex to wrap tightly around target protein

37
Q

enzyme-linked receptors

A

single span transmembrane
cytosolic domain has intrinsic enzymatic activity/ associated w enzyme

38
Q

RTK

A

Receptor tyrosine kinases
common enzyme-linked receptor
cytoplasmic domain has intrinsic kinase activity

39
Q

RTK examples

A

growth factor receptors (cell proliferation control)
insulin receptors (tetramers, binding causes realignment of polypeptide chains, activating cross-phosphorylation)

40
Q

binding of ligand to growth factor receptor

A

cross-linking of 2 receptor chains

41
Q

oligomerisation of receptor chains

A

allows cross/auto phosphorylation

42
Q

phosphorylated tyrosine residues

A

provide docking sites for other signalling proteins

43
Q

RAS

A

small monomeric G-protein/ proto-oncogene
main signal transducer protein for growth factors
activates downstream phosphorylation cascade for map kinase pathway

44
Q

% RAS mutations of cancers
% pancreatic

A

20-30% of cancers
80% pancreatic

45
Q

difference between trimeric and monomeric G-proteins

A

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
Q

GEF

A

Guanine nucleotide exchange factor

47
Q

GAP

A

GTPase activating protein

48
Q

RAS and GEF binding to RTK

A

mediated by Grb-2 adapter protein

49
Q

RAS mutation

A

affects GTP hydrolysis activity
GTP stays bound longer and signaling pathway continuously switched on
therefore cell proliferation occurs in absence of growth factors

50
Q

how can cells respond differently to the same signal

A

via different receptors
different intracellular machinery activation

51
Q

nicotinic ACh receptor

A

ion channel linked/ inotropic and fast
membrane depolarisation induces skeletal muscle contraction

52
Q

muscarinic ACh receptor

A

G-protein linked/ metabotropic and slow
hyperpolarisation of membrane reduces rate of contraction of heart muscle

53
Q

nitric oxide receptors

A

conformational change
produces c GMP as secondary messenger

54
Q

crosstalk

A

overlap between many different signalling pathways

55
Q

cross talk pro and con

A

:) allows fine-tuning of response
:( risk of producing wrong response

56
Q

types of crosstalk

A

additive (1+1=2)
synergism (1+1>2)
antagonism (1+1<2)

57
Q

3 types of signalling complexes

A

stable (components linked by scaffold protein)
transient (signalling complex assembles after receptor activated)
transient (modification of plasma phospholipid molecules)

58
Q

how to switch off signal

A

removal/ inactivation of signal/ receptor
inactivation of activated signal proteins
degradation of 2nd messengers

59
Q

removal of cell signal

A

degradation
recycling
sequestration

60
Q

what does rate of signal removal affect

A

response duration

61
Q

receptor removal

A

allows cell desensitization
involves ligand-dependent receptor-mediated endocytosis

62
Q

inactivation of activated proteins

A

GTP hydrolysis
dephosphorylation/ phosphorylation

63
Q

cholera toxin

A

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
Q

allosteric inactivation

A

dissociation from activator/ association w inhibitor

65
Q

removal of secondary messengers catalysis

A

phosphodiesterase

66
Q

viagra

A

inhibits cGMP phosphodiesterase so ^cGMP and prolonged muscle relaxation
competitive inhibitor

Cell biology semester 1 (6 decks)

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