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M&R > Receptors And Membrane Turnover > Flashcards

Receptors And Membrane Turnover Flashcards

0
Q

Define ligand

A

Any small molecule that binds specifically to a receptor site.

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1
Q

Define receptor

A

A molecule that recognises specifically a ligand or family of ligands, and in response to the ligand binding, brings about regulation of a cellular process.

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2
Q

What is an agonist

A

A ligand whose binding produces activation of a receptor.

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3
Q

What is an antagonist?

A

A ligand whose binding does not cause activation of and blocks a receptor.

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4
Q

Name the three types of chemical signals

A

Hormones, neurotransmitters, local chemical mediators

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5
Q

Where do the three types of chemical signals work?

A

Hormones - between cells in different tissues via the circulation
Neurotransmitters - at specialised cell junctions in the nervous system - synapses
Local chemical mediators - between adjacent cells in the same tissue

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6
Q

What is an acceptor?

A

When the basic function of a molecule can be carried out without the ligand. Its activity may just be modified by the ligand.

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7
Q

List the three ways of signal transduction for hydrophilic molecules

A

Integral ion channels
Membrane-bound receptors with integral enzyme activity
Membrane-bound receptors with transducing proteins

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8
Q

How do integral ion channels work?

A

Agonist binds to ligand-gated ion channel
Results in a conformational change and opening of a gated channel
Channel permits the flow of ions down an electrochemical gradient

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9
Q

Describe how membrane-bound receptors with integral enzyme activity work

A

Agonist binds to extracellular domain of the receptor
Causes a conformational change
Activates an intrinsic enzyme activity contained within the protein structure of the receptor

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10
Q

Structure of classical ligand-gated ion channel family?

A

Share similar pentameric subunits with four transmembrane domains

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11
Q

Example of classical ligand-gated in channels?

A

Nicotinic Ach receptors

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12
Q

Example of a non-classical ligand gated ion channel?

A

Ryanodine receptor (Ca2+)

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13
Q

How do tyrosine-kinase linked receptors work?

A

Binding of a hormone activates protein kinase activity in cytoplasmic domain of the receptor protein
It autophosphorylates tyrosine residues on that domain
Phosphorylated Tyr residues are recognised by transducing proteins or enzymes containing phosphotyrosine recognition sites
On association, these enzymes are activated allosterically, transducing the message into an intracellular event

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14
Q

Give an example of a tyrosine-kinase linked receptor

A

Insulin receptor

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15
Q

Describe the structure of membrane bound receptors wth transducing proteins

A

7 transmembrane domains coupled to effector molecules via a transducing molecule - a GTP-binding regulatory protein

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16
Q

What can the effectors be in a G-protein?

A

An ion channel

An enzyme eg adenylyl cyclase

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17
Q

What is integrated signalling?

A

When separate G-protein receptors act simultaneously to both stimulate/inhibit the effector

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18
Q

Give some examples of G-proteins

A

Muscarinic Ach receptors
Dopamine receptors
5-HT receptors
Light, smell and taste receptors

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19
Q

What are intracellular receptors bound to in their resting state?

A

Heat shock or chaperone proteins

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20
Q

What happens when an intracellular receptor is activated?

A

It dissociates from its stabilising protein and translocates to the nucleus where it binds to control regions of DNA, regulates gene expression

21
Q

Do intracellular receptors work faster of slower than the action of extracellular receptors?

A

Slower

22
Q

Why is molecular amplification needed?

A

The concentration of many extracellular signalling molecules is low

23
Q

How can amplification occur?

A

Molecule binds to a receptor
This stimulates the activity of an enzyme
This can cause the modification of hundreds of thousands of substrate molecules

24
Q

How can cardiac pacemaker cells be made to increase and slow heart rate

A

Noradrenaline binds to β1-adrenoreceptors which increases heart rate.

Ach binds to M2-muscarinic receptors which slows heart rate

25
Q

Describe phagocytosis

A

Ligand binds to receptors in the membrane of a cell
Cell extends pseudopods that permit further receptor interactions and membrane invagination via a membrane zippering mechanism
Internalised phagosomes fuse with lysosomes to form phagolysosomes in which the material is degraded

26
Q

What is pinocytosis?

A

The invagination of the plasma membrane to form a lipid vesicle.

27
Q

What does pinocytosis allow?

A

The uptake of impermeable extracellular salutes and retrieval of plasma membrane.

28
Q

What are the two forms of pinocytosis?

A

Fluid phase

Receptor-mediated endocytosis

29
Q

What happens in receptor mediated endocytosis?

A

Specific binding of molecules to cell surface receptors permits the selective intake of substances into the cell

30
Q

Structure of LDLs?

A

A core of cholesterol molecules esterified to fatty acids.

Surrounded by a lipid monolayer containing phospholipids, cholesterol and apoprotein B

31
Q

What are Clathrin-coated pits?

A

Clusters of receptors that cells produce when they require cholesterol. They form spontaneously
They recognise specifically apoprotein B

32
Q

What happens when LDL binds to the receptors?

A

The pit invaginates to form coated vesicles.
The vesicles are then uncoated in a process which requires ATP and they fuse with larger, smooth vesicles called endosomes

33
Q

Why is the enzyme known as a Compartment for Uncoupling of Receptor and Ligand? (CURL)

A

The endosome has a lower pH than the cytoplasm

At this pH, the LDL has a lower affinity for the particle and the two dissociate

34
Q

How is the pH of the endosome maintained?

A

By an ATP-dependent proton pump

35
Q

What happens to the LDL-receptor after it has dissociated in the endosome?

A

They are sequestered to a domain of the endosome membrane which buds off as a vesicle and recycles the LDL receptor to the plasma membrane.

36
Q

What happens to the endosomes containing the LDL?

A

Fuse with lysosomes.

Cholesterol is hydrolysed from the esters and released into the cell

37
Q

What are the three mutations affecting LDL-receptors in hypercholesterolaemia?

A

Non-functioning receptor
Receptor binding normal
Receptor deficiency

38
Q

In hypercholesterolaemia, what happens in a non-functioning receptor?

A

Mutation in LDL binding site of LDL receptor prevents binding of LDL and its uptake

39
Q

What happens in a receptor binding normal mutation in hypercholesterolaemia?

A

Mutation can cause deletion of the C terminal cytoplasmic domain. This prevents interaction between the receptor and the Clathrin coat. LDL receptor are distributed over the entire cell surface.

40
Q

What happens in the receptor deficiency mutation in hypercholesterolaemia?

A

Prevents expression of the LDL receptor

41
Q

What do iron ions bind to and what does this produced?

A

Two Fe3+ ions bind to apoptransferrin to form transferrin

42
Q

What does transferrin do?

A

Binds to the transferrin receptor at neutral pH and is internalised in a similar way to LDL.

43
Q

What happens after the transferrin gets to the endosome?

A

Has a lower pH
The fe3+ ions are released from the transferrin but at this pH, the apoptransferrin remains associated with the transferrin receptor
Complex is sorted in the CURL for recycling back to the plasma membrane
At pH 7.4, the apoptransferrin dissociates from the receptor

44
Q

How are insulin receptors taken up?

A

Insulin-binding induces a conformational change in the receptor that allows it to be recognised at the pit.
In the endosome, insulin remains bound to the receptor and the complex is targeted to the lysosomes for degradation.

45
Q

Why does a continued high concentration of insulin lead to desensitisation of a cell to insulin?

A

Because the receptor is degraded after it has been used. Fewer receptors for insulin binding

46
Q

Give two examples of ligand transcytosis

A

The transfer of maternal immunoglobulins to the foetus via the placenta
Transfer of immunoglobulin A from the circulation to bile in the liver.

47
Q

What is the fate of the ligand and receptor in uptake of cholesterol?

A

Ligand is degraded

Receptor is recycled

48
Q

What is the fate of receptor and ligand in uptake of iron ions by transferrin?

A

Both are recycled

49
Q

What is the fate of the ligand and receptor for insulin, epidermal growth factor and immune complexes?

A

Both are degraded

50
Q

List 3 members of the classical ligand-gated ion channel receptor family

A

GABA receptor type A
Glycine receptor
nAchR

M&R (10 decks)

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