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ESA 2- Membranes and Receptors > Receptors and Membrane Turnover > Flashcards

Receptors and Membrane Turnover Flashcards

1
Q

What is a receptor?

A

A molecule that recognises specifically a second molecule (ligand), or family of molecules, and in response to binding brings about the regulation of a cellular process

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2
Q

How are receptors classified?

A

Primarily by their specificity to a physiological signalling molecule.
Often further divided on the basis of their affinity to a series of antagonists

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3
Q

How does the affinity of ligand binding at receptors differ from binding to substrates to enzyme sites? Why?

A

Much higher

Ligands may only be present in very small concentrations

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4
Q

What are the roles of receptors?

A

Include signalling via hormones, neutrotransmission, cellular delivery and many more

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5
Q

What must be true of a receptor at rest?

A

It must be silent

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6
Q

What is an acceptor?

A

A molecule that operates in the absence of it’s ligand

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7
Q

What is a ligand?

A

Any molecule that binds specifically to a receptor site

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8
Q

What is an agonist?

A

A ligand that produces activation of the receptor on binding

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9
Q

What is an antagonist?

A

A receptor that binds without causing activation, blocking the receptor

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10
Q

What do small, hydrophobic signalling molecules do?

A

Pass through the cell membrane and bind to receptors inside of cells

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11
Q

What may small, hydrophobic molecules have?

A

Carrier proteins that they bind to whilst travelling in the blood

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12
Q

What is needed for the binding of hydrophilic signalling molecules that can’t pass through the cell membrane?

A

Signal transduction

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13
Q

How is signal transduction bought about?

A

With the presence of an extracellular receptor at the cell surface, which then transmits the signal into the cell

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14
Q

How can membrane bound receptors achieve transmission of a signal into the cell?

A

Intergral ion channels
Integral ion channels
Coupling to effectors through transducing proteins

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15
Q

What does agonist binding to a ligand-gated ion channel result in?

A

A conformational change, and the opening of a gated channel

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16
Q

What is the result of an agonist opening an ion channel?

A

The channel then permits the flow of ions down an electrochemical gradient

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17
Q

What family do several of the membrane bound receptors with integral ion channels belong to?

A

The classical ligand-gated ion channel family

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18
Q

What do the classical ligand-gated ion channel family have in common?

A

They share similar pentameric subunit structures with four transmembrane domains

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19
Q

Give an example of a classical ligand-gated ion channel receptor

A

Nicotinic ACh receptor (NAChR)

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20
Q

Give an example of a non-classical ligand-gated ion channel

A

Ryanodine receptor

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21
Q

What does agonist binding to the extracellular domain of membrane bound receptors with integral enzyme activity cause?

A

A conformational change, which activates an intrinsic enzyme activity, contained within the protein structure of the receptor

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22
Q

Give an example of a membrane bound receptor with integral enzyme activity?

A

Tyrosine kinase linked receptors

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23
Q

What do tyrosine kinase linked receptors do?

A

Autophosphorylate upon ligand binding

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24
Q

What are phosphorylated receptor tyrosine residues recognised by?

A

Either by transducing proteins or directly by enzymes containing phosphotyrosine recognition sites, src-homology-2 domains

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25
Q

Give an example of a transducing protein that recognises phosphorylated tyrosine residues

A

Insulin receptor substrate-1

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26
Q

What happens to effector enzymes on association with receptor or transducing proteins?

A

They become activated

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27
Q

How does association of an enzyme with a receptor or transducing protein activate it?

A

Either allosterically or by tyrosine phosphorylation by the receptor kinase

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28
Q

What happens on the activation of an effector enzyme?

A

It transduces the message into an intracellular chemical event

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29
Q

What are the G-protein coupled receptors?

A

A family of receptors that have seven transmembrane domain receptors that couple to effector molecules via a transducing molecule, a GTP-binding regulatory protein (G-protein)

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30
Q

What can the effector molecules to G-proteins be?

A

Enzymes or ion channels

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31
Q

Give 6 examples of extracellular signalling molecule receptors that have a structure including seven transmembrane domains?

A 
Muscarinic ACh receptors
 Dopamine receptors
 5-HT receptors
 Light receptors
 Smell receptors
 Taste receptors
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32
Q

What often exists for a particular agonist?

A

A number of different types of G-protein receptors

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33
Q

How will separate G-protein receptors often act?

A

Simultaneously, to both stimulate/inhibit the effector

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34
Q

What is it called when separate G-protein coupled receptors act simultaneously?

A

Integrated signalling

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35
Q

What produces the outcome in integrated signalling?

A

The two inputs combine to produce a measured effect

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36
Q

Give 5 examples of hydrophobic ligands

A

The steroid hormones cortisol, oestrogen and testosterone, and the thyroid hormones T3 and T4

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37
Q

How do hydrophobic ligands get through the plasma membrane?

A

They can pass through

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38
Q

What do hydrophobic ligands bind to?

A

Receptors inside the cell

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39
Q

What happens to intracellular receptors in their resting state?

A

They are bound to heat shock or chaperone proteins

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40
Q

What happens to an activated intracellular receptor?

A

It dissociates from the stabilising protein and translocated to the nucleus

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41
Q

What happens to an activated receptor once it has translocated to the nucleus?

A

It binds to control regions in DNA

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42
Q

What is the result of the binding of receptors to control regions of DNA?

A

It regulates gene expression

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43
Q

How does the action of intracellular receptors compare to extracellular receptors?

A

It is relatively slow

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44
Q

Why is the action of intracellular receptors relatively slow?

A

They are dependant on transcription and translation

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45
Q

What is the concentration of many extracellular signalling molecules?

A

Very low

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46
Q

What is possible with each mechanism of cellular signalling?

A

Molecular amplification

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47
Q

Give an example of the effect molecular signalling can have

A

By stimulating the activity of an enzyme, the binding of a chemical signal molecule to a single receptor can cause teh modification of hundreds of thousands of substrate molecules

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48
Q

What can an enzymatic cascade produce?

A

Further amplification

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49
Q

What effect does noradrenaline have on the heart rate?

A

Increases it

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50
Q

How does noradrenaline exert its affect on the cardiac pacemaker cells?

A

Through ß1-adrenoreceptors

51
Q

What is the effect of acetylcholine on the heart rate?

A

Decreases it

52
Q

How does acetylcholine exert its effect on the cardiac pacemaker cells?

A

Through M2-Muscarinic receptors

53
Q

Where does phagocytosis occur in mammals?

A

Only in specialised cells

54
Q

What cells conduct phagocytosis?

A

Macrophages

Neutrophils

55
Q

Describe the process of phagocytosis

A

In response to the binding of a particle to receptors in the plasma membrane, the cell extends psuedopods that permits further receptor interactions and membrane invagination/particle internalisation, via a ‘membrane zippering’ mechanism. Internalised phagosomes fuse with lysosomes to form phagolysosomes in which the particulate material is degraded

56
Q

What does the phagocytosis process permit?

A

The clearance of damaged cellular materials and invading organisms for destruction

57
Q

What is pinocytosis?

A

The invagination of the plasma membrane to form a lipid vesicle

58
Q

What does pinocytosis permit?

A

The uptake of impermeable extracellular solutes and retrieval of plasma membrane

59
Q

What forms can pinocytosis be sub-divided into?

A

Fluid-phase

Receptor mediated endocytosis

60
Q

What happens in receptor mediated endocytosis?

A

Specific binding of molecules to cell surface receptors

61
Q

What does receptor mediated endocytosis permit?

A

Selective uptake of substances into the cell

62
Q

Where do low-density lipoproteins (LDLs) originate from?

A

The liver

63
Q

What do LDLs consist of?

A

A core of cholesterol molecules esterified to fatty acid, surrounding by a lipip monolayer containing phospholipids, cholesterol and a single protein species, apoproteinB

64
Q

What do animal cells that require cholesterol synthesise/

A

Surface LDL-receptors that recognise specifically apolipoprotein B

65
Q

Where are the LDL-receptors that recognise specifically apolipoproteinB found?

A

They are localised in clusters over clathrin coated pits

66
Q

What % of the cell surface is covered by clathrin coated pits?

A

Approx 2%

67
Q

When do clathrin coated pits form?

A

Spontaneously

68
Q

What does clathrin spontaneously form?

A

Cages

69
Q

What happens when LDL binds to its receptor?

A

The pit invaginates to form coated vesicles

70
Q

How are vesicles uncoated?

A

In a process that requires ATP

71
Q

Why does the uncoating process require ATP?

A

As coat formation is spontaneous

72
Q

What happens once the vesicles have been uncoated?

A

They fuse with larger, smooth vesicles called endosomes

73
Q

What is the pH of the endosome?

A

5.5-6.0

74
Q

How does the pH of the endosome compare to that of the cytoplasm?

A

It is lower

75
Q

What is the pH of the endosome maintained by?

A

By an ATP-dependant proton pump

76
Q

What is the affinity for the LDL particle for the LDL receptor for the pH of the endosome?

A

Low

77
Q

What is the result of the low affinity of the LDL receptor to the LDL particle at the pH of the endosome?

A

The two dissociate

78
Q

What is the result of the pH of the endosome causing dissociation of the LDL receptor and particle?

A

It is known as the compartment for the uncoupling of receptor and ligand

79
Q

How is the LDL-receptor recycled to the plasma membrane?

A

The receptors are sequestered to a domain within the endosome membrane, which buds off as a vesicle
May go via the Golgi apparatus

80
Q

How is cholesterol released into the cell?

A

The endosomes containing the LDL fuse with lysosomes, and the cholesterol is hydrolysed from the esters and released into the cell

81
Q

What mutations can cause hypercholesterolaemia?

A

Non-functioning receptor
Deletion of the C-terminal cytoplasmic domain
Receptor deficiency

82
Q

What happens if there is a mutation of the LDL binding site of the LDL-receptor?

A

It will prevent the binding and uptake of LDL

83
Q

What happens if there is a deletion of the C-terminal cytoplasmic domain?

A

It prevents the interaction between the receptor and Clathrin coat, and so the LDL receptors will be distributed over the entire cell surface instead of being concentrated in 2% of the cell

84
Q

What causes a receptor deficiency?

A

A mutation that prevents expression of the LDL-receptor

85
Q

Describe the process of Fe ion uptake by transferrin?

A

Two Fe ions bind to Apoptransferrin to form transferrin in the circulation.
Transferrin binds to the transferrin receptor at neutral pH and is internalised.
Upon reaching the acidic endosome, the Fe ions are released from the transferrin, but at this pH apotransferrin remains associated with the transferrin receptor
The complex is sorted in the CURL for recycling back to the plasma membrane, where at pH 7.4 the apoptransferrin dissociates from the receptor again

86
Q

When do insulin receptors congregate over Clathrin coated pits?

A

Only when their agonist is bound

87
Q

What does insulin binding induce in the receptor?

A

A conformational change

88
Q

What is the result of the induced conformational change in the insulin receptor?

A

It allows it to be recognised by the pit

89
Q

What happens to the insulin-receptor complex in the endosome?

A

It remains bound to the receptor

The complex is targeted to the lysosomes for degradation

90
Q

What does the mechanism of occupied insulin receptors allow for?

A

Reduction in the number of insulin receptors on the membrane surface, desensitising the cell to a continued presence of high circulating insulin concentration

91
Q

What may happen to some ligands that remain bound to their receptors?

A

They may be transported across the cell

92
Q

What is the process of transport across the cell called?

A

Transcytosis

93
Q

Give 2 examples of where transcytosis occurs?

A

Maternal immunoglobulins to the foetus via the placenta

Transfer of immunoglobulin A (IgA) from the circulation to bile in the liver

94
Q

What happens during transport of IgA?

A

The receptor is cleaved, resulting in the release of immunoglobulin with a bound ‘secretory component’ derived from the receptor

95
Q

How do receptors for different ligands enter the cell?

A

Via the same Clathrin coated pits

96
Q

How does the pathway from coated pits to the endosome differ in protein that undergo endocytosis?

A

It doesn’t!!!!! ha ha trick question lol

97
Q

How can different modes of the process of receptor-mediated endocytosis be defined?

A

On the basis of the destination of the internalised receptor and ligand

98
Q

How are receptors targeted to different cellular destinations?

A

By short amino acid motifs

99
Q

Where are receptors targeted to different cellular destinations sorted?

A

Within the CURL

100
Q

What happens to receptors targeted to targeted to different cellular locations once they have been sorted?

A

They are sorted to discrete regions of membrane, and bud off into transport vesicles

101
Q

How many modes of receptor mediated endocytosis are there?

A

4

102
Q

What happens to the receptor in mode 1 of receptor mediated endocytosis?

A

It is recycled

103
Q

What happens to the ligand in mode 1 of receptor mediated endocytosis?

A

It is degraded

104
Q

Give an example of something that uses mode 1 of receptor mediated endocytosis?

A

LDL

105
Q

What is the function ofmode 1 of receptor mediated endocytosis?

A

Metabolite uptake

106
Q

What happens to the receptor inmode 2 of receptor mediated endocytosis?

A

It is recycled

107
Q

What happens to the ligand inmode 2 of receptor mediated endocytosis?

A

It is recycled

108
Q

Give an example of something that usesmode 2 of receptor mediated endocytosis?

A

Transferrin

109
Q

What is the function ofmode 2 of receptor mediated endocytosis?

A

Metabolite uptake

110
Q

What happens to the receptor inmode 3 of receptor mediated endocytosis?

A

It is degraded

111
Q

What happens to the ligands inmode 3 of receptor mediated endocytosis?

A

Degraded

112
Q

Give 3 examples of things that usemode 3 of receptor mediated endocytosis

A

Insulin
Epidermal growth factor
Immune complexes

113
Q

What is the function ofmode 3 of receptor mediated endocytosis?

A

Receptor down-regulation

Removal from circulation of foreign antigen

114
Q

What happens to the receptor inmode 4 of receptor mediated endocytosis?

A

Transported

115
Q

What is ligand inmode 4 of receptor mediated endocytosis?

A

Transported

116
Q

Give 3 examples of things that usemode 4 of receptor mediated endocytosis?

A

Maternal IgA

IgA

117
Q

What is the function ofmode 4 of receptor mediated endocytosis?

A

Transfer of large molecules across the cell

118
Q

What can exploit endocytic pathways to enter cells?

A

Membrane-enveloped viruses and some toxins

119
Q

What must happen for exploitation of endocytic pathways into cells?

A

Adventitious binding to receptors in the plasma membrane

120
Q

What happens to membrane-enveloped viruses and some toxins once in the endosome?

A

The acidic pH allows the viral membrane to fuse with the endosomal membrane

121
Q

What happens when the viral membrane can fused with the endosomal membrane?

A

It releases the viral RNA into the cell where it can be translated and replicated by the host cell’s machinery to form new viral particles

122
Q

Give 2 examples of toxins that exploit endocytic pathways to enter cells?

A

Cholera toxin

Diphtheria toxin

123
Q

What do cholera and diphtheria toxins bind to?

A

GM1 ganglioside

ESA 2- Membranes and Receptors (13 decks)

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