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Semester 2 > M&R Session 7 > Flashcards

M&R Session 7 Flashcards

0
Q

By what two mechanisms can cell surface receptors act?

A

Directly alter cellular activity

Transduction of initial binding event via other intracellular components

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1
Q

What tends to happens to cells if they do not receive extracellular signals?

A

They die

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2
Q

What cellular activity can be controlled by transduction of initial binding event?

A

Contraction
Secretion
Proliferation
Differentiation

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3
Q

What are the three superfamilies of cell-surface receptors?

A

Ligand-gated (receptor operated) ion channels
Receptors w/intrinsic enzymatic activity
GPCRs

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4
Q

Which superfamily of cell-surface receptors is heterogenous?

A

Receptors w/ intrinsic enzyme activity

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5
Q

Describe the mechanism of receptors w/intrinsic enzyme activity.

A

Ligand binding activates an enzyme

Enzyme phosphorylates the receptor itself and other substrates

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6
Q

Which superfamily of cell-surface receptors do insulin receptors belong?

A

Receptors w/intrinsic enzyme activity

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7
Q

How do GPCRs have specificity of action?

A

Each receptor subtype is specific for one/ limited number of endogenous ligands

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8
Q

What is an agonist?

A

A molecule that binds to a GPCR and activates it causing intracellular signal transduction events

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9
Q

What drugs are used to treat asthma?

A

Beta-2 adrenoreceptor agonists

E.g. Salbutamol, Salmeterol

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10
Q

What type of molecules are used for analgesia/anaesthesia?

A

Mu-opioid receptor agonists

E.g. Morphine, Fentanyl

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11
Q

What are antagonists?

A

Molecules that bind to a receptor but do not activate it; they block the effects of agonists

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12
Q

What type of molecules are used to treat hypertension?

A

Beta-adrenoreceptor antagonists

E.g. Propanolol, Atenolol

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13
Q

What are Haloperidol and Sulpiride examples of?

A

Anti-schizophrenic D2 dopamine receptor antagonists

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14
Q

What effect do antagonists have on certain mechanisms?

A

Damp-down hyper activation

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15
Q

Give the key features of GPCR structure.

A 
300-1200 a.a. chain
7TMD
2 regions for ligand binding: in TMD or N-terminal region
Extracellular N-terminal
Intracellular C-terminal
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16
Q

What can drugs targeting GPCRs be used to treat?

A 
Parkinson's disease
Congestive heart failure
Thrombosis
Benign prostatic hyperplasia
Acid reflux
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17
Q

What two types of mutation can occur to cause a disease associated w/signal transduction?

A

Loss of function

Gain of function

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18
Q

What causes retinitis pigmentosa?

A

Loss of function rhodopsin mutation

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19
Q

What causes nephrogenic diabetes insipidus?

A

Love of function mutation of V2 vasopressin receptor

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20
Q

What happens in a gain of function mutation?

A

Receptor becomes independent of ligand –> endocrine changes

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21
Q

What causes familial male precocious puberty?

A

LH receptor mutation

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22
Q

What stimuli can GPCRs respond to?

A 
Light, odour, taste
Ions
Neurotransmitters
Hormones
Large glycoproteins
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23
Q

How do GPCRs cause a change in cellular activity?

A

Ligand binds –> conformational change –> GPCR activated –> interacts w/guanine-nucleotide binding protein –> activates G-protein –> GDP replaced by GTP on alpha-subunit

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24
Q

What is the structure of a guanine-nucleotide binding protein?

A

Heterotrimeric

Alpha, beta and gamma subunits

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25
Q

Why is a G-protein functionally dimeric?

A

Once the beta and game subunits are synthesised they stick together

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26
Q

What is the function of the alpha subunit of a G-protein?

A

Bind to guanine nucleotide

GTPase activity

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27
Q

When does GTP have a natural tendency to bind to the alpha subunit?

A

When the binding site is empty

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28
Q

How do you activate a G-protein?

A

Guanine nucleotide exchange by replacing GDP w/GTP

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29
Q

How do you turn off a G-protein?

A

Hydrolyse GTP

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30
Q

Which subunits can interact w/effector proteins?

A

Alpha

Beta-gamma

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31
Q

What effector proteins can the G-protein subunits interact with?

A

2nd messenger generating enzymes

Ion channels

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32
Q

What is amplification governed by?

A

Timer function of the G-protein unit

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33
Q

What is timer function?

A

Capacity of how long the signal can be passed on for by a GPCR

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34
Q

Why can efficiency of signal transmission be targeted therapeutically?

A

In different pathways it can be altered

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35
Q

What is the primary determinant of receptor G-protein selection?

A

The ~20 different G-alpha proteins in the human genome

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36
Q

Does a GPCR have its own unique G-protein combination?

A

No

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37
Q

How many possible G-alpha-beta-gamma protein combinations are possible in the human genome?

A

> 1000

38
Q

How is a specific cellular response brought about by a GPCR?

A

An extracellular signal working via a specific GPCR will activate a single/small sub-population of G-proteins and effectors in the cell

39
Q

What is the ligand, G-protein and effector for beta-adrenoreceptors?

A

Adrenaline/NA
Gs-alpha
+ adenylyl cyclase

40
Q

What is the ligand, G-protein and effector for alpha-2-adrenoreceptors?

A

Adrenaline/NA
Gi-alpha
- adenylyl cyclase

41
Q

What GPCR, ligand and effector are used for Gq-alpha proteins?

A

Alpha-1-adrenoreceptors
Adrenaline/NA
+ phospholipase C

42
Q

What ligand, GPCR and G protein are used to stimulate cyclic GMP phosphodiester Awe?

A

Light
Rhodopsin
Gt-alpha

43
Q

What ligand acts at M2/4 muscarinic GPCRs?

A

ACh

44
Q

What G-proteins are used for M2/4 muscarinic receptors?

A

Gi-alpha

45
Q

What effector does Gi-alpha activation act on?

A

-adenylyl cyclase

46
Q

What ligand, G-protein and effector do M1/3 GPCRs use?

A

ACh
Gq-alpha
+ phospholipase C

47
Q

Which pathway do even numbered muscarinic receptors follow the same as?

A

Alpha-2-adrenoreceptors

48
Q

Which pathway do odd numbered muscarinic receptors follow the same as?

A

Alpha-1-adrenoreceptors

49
Q

Name two ADP-ribosylate specific G-proteins.

A

Cholera toxin

Pertussis toxin

50
Q

What mechanism of action does cholera toxin use?

A

Eliminates GTPase activity of Gs-alpha

Irreversibly activates Gs-alpha

51
Q

How does cholera toxin irreversibly activate Gs-alpha?

A

ADP-ribosylation of the unit prevents deactivation of Gs protein mediated signalling

52
Q

Cells in which area of the body are infected by cholera toxin?

A

Small intestine

53
Q

What happens to the toxin complex in both cholera and pertussis toxin action?

A

It binds to the cell and the emzyme is ‘injected’ into the cell

54
Q

What type of cell does Bordetella pertussis bacteria colonise?

A

Tracheal epithelial

55
Q

What characteristic symptom does pertussis toxin cause?

A

Whooping cough

56
Q

By what method of action does pertussin toxin cause whooping cough?

A

Interferes w/ GDP-GTP exchange so Gi-alpha is irreversibly inactivated

57
Q

How does pertussis toxin cause irreversible inactivation of Gi-alpha?

A

ADP-ribosylation of the subunit prevents Gi protein activation by GPCRs

58
Q

What is PIP3?

A

A more phosphorylated form of the membrane phospholipid PIP2 that regulates a variety of processes - often survival signals

59
Q

How is adenylyl cyclase regulated by agonist stimulation?

A

Ligand on receptor activates G-protein –> guanine nucleotide transfer –> activated Gs-alpha –> stimulates adenylyl cyclase –> secondary messenger cAMP formed

60
Q

Which receptors are Gs coupled receptors?

A

Beta-adrenoreceptors
D1 dopamine receptors
H2 histamine receptors

61
Q

Which receptors are Gi coupled receptors?

A

Alpha 2-adrenoreceptors
D2 dopamine receptors
My-opioid receptors

62
Q

What does cAMP act on?

A

cAMP-dependent protein kinase A (PKA)
Epacs (GEFs)
Cyclic-nucleotide-gated ion channels (CNGs)

63
Q

Describe the structure of PKA.

A

2 regulatory subunits sat in active site of 2 catalytic subunits

64
Q

How does cAMP activate PKA?

A

Binds to regulatory subunits –> catalytic subunits dissociate exposing active site –> catalytic subunits phosphorylate specific target proteins in the cell that have serine or threonine residues

65
Q

How is phospholipase C regulated by agonist stimulation?

A

Ligand on receptor activates G-protein –> guanine nucleotide transfer –> activated Gq-alpha –> stimulates PLC –> PIP2 into IP3 and DAG

66
Q

Which part of the PIP2 molecule forms IP3?

A

Polar head group

67
Q

Which part of the PIP2 molecule forms DAG?

A

Lipid moiety

68
Q

What intracellular affect does IP3 have?

A

It releases calcium ions

69
Q

What affect does DAG have?

A

Acts on PKC which can act on lots of different molecules to affect activity

70
Q

Which receptors are Gq coupled receptors?

A

Alpha 1-adrenoreceptors
M1 muscarinic receptors
H1 histamine receptors

71
Q

What is the advantage of signal amplification?

A

Modest concentration changes cause significant effects within cell

72
Q

What affect does a few hundred molecules of adrenaline binding to cell surface beta-adrenoceptors have?

A

Glycogenolysis in the liver causing milimolar changes in blood glucose concentration

73
Q

What magnitude of amplification does adenylyl cyclase itself cause?

A

Little

74
Q

What follows activation of adenyly cyclase?

A

Lots of cAMP molecules released which activate PKA

75
Q

Which two molecules cause ventricular mass to contract more forcefully?

A

Blood-borne adrenaline

Sympathetically released NA

76
Q

Which receptors are activated to cause increased for of ventricular contraction?

A

Beta 1-adrenoreceptors

77
Q

What is an increase in the force of contraction also called?

A

+ve inotropy

78
Q

What causes an increase in the force of contraction?

A

VOCC phosphorylation by PKA –> each depolarisation allows in slightly more calcium than usual –> triggers CICR

79
Q

What do sympathetically released NA and some blood-borne adrenaline interact with to cause vasoconstriction?

A

Alpha 1-adrenoreceptors

80
Q

What causes bronchoconstriction?

A

Parasympathetic Ach action on M3-muscarinic receptors

81
Q

What causes GI and GU smooth muscle contraction?

A

A variety of agents on GPCRs

82
Q

What mechanism do all methods of regulation of smooth muscle tone utilise?

A

Gq-phospholipase C-IP3/Ca2+, DAG/protein kinase C pathways

83
Q

What allows for coordinated increase in contractility of smooth muscle?

A

Utilisation of the same pathways

84
Q

What often modulates neurotransmitter release in the CNS and PNS?

A

Pre-synoptic GPCRs

85
Q

What is encephalin?

A

An endogenous ligand

86
Q

What receptors do morphine and encephalin bind to?

A

Mu-opioid

87
Q

Which subunit has most affect in the activation of mu-opioid receptors?

A

G-beta-gamma

88
Q

What action does the g-beta-gamma subunit have?

A

Causes modulating inhibition of specific types of VOCC (very different to those in the heart)

89
Q

What causes turned down neurotransmitter release?

A

Decreased calcium influx from specific VOCC modulating inhibition causing reduced vesicle docking

90
Q

What allows for diversity in effector mechanisms of signal transduction?

A

Range of stimuli
Receptors
G-proteins
Effectors

91
Q

What gives specificity of effector mechanisms in signal transduction?

A

Specific ligand-receptor interactions
Specific G-alpha subunits recruited coupled to particular effector pathways - different between cells but hard wired so that in the same cell type they have the same response

92
Q

What benefit does amplification give to signal transduction?

A

Allows for gain of control on signalling pathways

Semester 2 (45 decks)

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