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ESA2 > MR S6 - Receptors & Membrane Turnover > Flashcards

MR S6 - Receptors & Membrane Turnover Flashcards

0
Q

State a few roles of receptors

A 
Signalling via:
Hormones
Neurotransmission
Cellular delivery
Ect
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1
Q

What is a receptor?

A

A molecule which specifically binds to another molecule to illicit a change in a cellular process

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2
Q

What is a ligand?

A

Any molecule that binds specifically to a receptor site

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3
Q

What is an agonist?

A

A ligand which binds to a receptor and causes activation of that receptor

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4
Q

What is an antagonist?

A

A ligand which binds to a receptor and doesn’t cause activation of that receptor

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5
Q

What is signal transduction?

A

The transmission of a signal inside the cell when a ligand binds to a receptor on the cell surface

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6
Q

How may a signal be transduced?

A
  • Integral ion channels
  • Integral enzyme activity
  • Coupling to effectors through transducing proteins
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7
Q

Why is signal transduction necessary?

A

To propagate the signal within the cell - hydrophilic ligands cannot pass the cell membrane so signal transduction is required

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8
Q

Describe membrane transduction by integral ion channels

A

Agonist binding causes conformational change and the opening of a gated channel
Channel then permits the movement of ions down their concentration gradient
Eg classical nAChr and non classical Ryanodine receptors

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9
Q

Describe membrane receptors with integral enzyme activity

A

Agonist binding to the extracellular domain causes conformational change
This activates an enzyme which form a part of the protein structure
Eg PDGF and linked tyrosine kinase

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10
Q

Describe tyrosine linked receptors

A

Autophosphorylate upon ligand binding
Residues recognised by transducing proteins or directly by enzymes
Upon association, effector enzymes are activated which transduce the message into an intracellular chemical event
Eg insulin receptor

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11
Q

Describe membrane bound receptors with transducing proteins

A

This family of receptors are known as GPCRs
7 transmembrane domain receptors couple to effector molecules via a transducing protein: a GTP binding regulatory protein or G protein
Effectors may be enzymes or ion channels

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12
Q

What is integrated signalling?

A

When separate GPCRs act simultaneously to stimulate or inhibit an effector
The two inputs combine to produce a measured effect

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13
Q

Give examples of GPCRs

A

Dopamine receptors, mAChR, 5-HT receptors and light, smell and taste receptors

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14
Q

Describe the specificity of GPCRs in relation to their distribution

A

Very specific
Several GPCRs can exist for the same agonist
Eg M1-5 ACh receptors - each type are found in different locations.
Useful as drugs can be targeted at one type of GPCR to only affect a local area.

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15
Q

Give examples of hormones with intracellular receptors

A 
Hydrophobic hormones eg:
Oestrogen
Testosterone
T3 & T4
Cortisol
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16
Q

Describe binding to intracellular receptors

A

Hydrophobic ligands pass through the cell membrane
Bind to intracellular receptors (in resting state these are bound to heat shock or chaperone proteins)
Activated receptor dissociates from it’s stabilising protein and moves to the nucleus where it binds to control regions in DNA

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17
Q

What is a disadvantage of intracellular receptors?

A

They bind to DNA so they change translation and/or transcription therefore they have a slower effect than extracellular receptors

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18
Q

How does amplification of signalling molecules occur?

A

Many ways eg
Stimulation of an enzyme can cause the binding of a single molecule to be amplified to hundreds or thousands of molecules
Enzyme cascades can be triggered, causing further amplification

19
Q

Why may amplification of cellular signals be necessary?

A

The concentrations of extracellular signalling molecules can be very low so amplification may be needed to trigger an appropriate response

20
Q

In cardiac pacemaker cells, stimulation of which receptors cause increase and decrease of heart rate?

A

Increase: β1 adrenoreceptors are activated by noradrenaline
Decrease: M2 muscarinic receptors are activated by acetylcholine

21
Q

In hepatocytes, how does hormonal stimulation affect glycogen stores?

A

Insulin binding to receptors stimulates glycogen synthesis

Glucagon binding to receptors stimulates glycogen breakdown

22
Q

Describe phagocytosis

A

A particle binds to a receptor on the cell membrane
The cell extends pseudopods to invaginate the particle with a membrane zippering mechanism
Internalised phagosomes fuse with lysosomes to form phagolysosomes in which the particle is degraded

23
Q

What is pinocytosis?

A

The invagination of the plasma membrane to form a lipid vesicle
Permits uptake of impermeable extracellular solutes and retrieval of plasma membrane
Sub divided into fluid phase and receptor mediated endocytosis (RME)

24
Q

Describe receptor mediated endocytosis (RME)

A

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

25
Q

Describe the uptake of cholesterol as an example of RME

A

LDL binds to apoprotein B receptor in clathrin pit on target cell surface
Pit invaginates to form coated vesicles
Coated vesicles are actively (aka using ATP) uncoated
They then fuse with endosomes
LDL particle and receptor dissociate
Receptor is recycled and returns to plasma membrane
Endosome fuse with lysosomes
Cholesterol is hydrolysed from the esters and released into the cell

26
Q

Describe the structure of an LDL

A

Core of fatty acids (esterified cholesterol)

Lipid mono layer of phospholipids, cholesterol and apoprotein B

27
Q

How is cholesterol only absorbed by cells that require it?

A

The target cells have apoprotein B receptors located in clathrin coated pits which spontaneously form on the cell membrane
These pits cover ~2% of the cell surface

28
Q

Why do the LDL receptors and particles dissociate in the endosome?

A

The pH is lower within the endosome than in the cytoplasm (5.5-6.0)
This means the receptor and particle have a lower affinity for each other

29
Q

What is an endosome also known as and why?

A

A CURL
Compartment for the Uncoupling of Receptor and Ligand
This is where the receptor and ligand uncouple

30
Q

What are the different ways the LDL receptor can be affected in hypercholesterolaemia?

A

Non-functioning receptor
C-terminal mutation
Receptor deficiency

31
Q

What would be the effect of a mutation to the binding site of an LDL receptor?

A

A mutation in the binding site could change the conformation so the receptor can no longer bind to the LDL so no uptake of LDL therefore LDL receptor os non functional

32
Q

What would be the effect of a mutation to the C-terminal of an LDL receptor?

A

The receptor interacts with clathrin with it’s c terminal domain
If there is a deletion of the C-terminal domain, the receptor can’t interact with clathrin
Therefore the receptors will be spread out across the membrane instead of in the 2% of the membrane where there are clathrin pits

33
Q

How may a receptor deficiency be caused?

A

By a mutation which prevents expression of the LDL receptor

Eg a start codon deletion

34
Q

Describe the uptake of Fe3+ ions as an example of RME

A

Two Fe3+ ions bind to apoptransferrin to form transferrin in the circulation
Transferrin binds to it’s receptor on the cell surface
Upon reaching the acidic endosome, the Fe3+ ions release
The complex is sorted for recycling back to the plasma membrane where the apoptransferrin dissociates from the receptor

35
Q

Why does the receptor-apoptransferrin complex only dissociate at the membrane?

A

Affinity at neutral pH is greatly reduced so it is only at the membrane that the apoptransferrin dissociates from the receptor

36
Q

Describe the uptake of occupied insulin receptors

A

When occupied, the insulin receptors gather over clathrin pits
Upon insulin binding, the pit invaginates to form a coated vesicle
The vesicle is actively uncoated and fuses with an endosome
At the endosome, the insulin-receptor complex remains associated
The endosome fuses with a lysosome and both ligand and receptor are degraded

37
Q

What are the three steps of RME that are common to all examples?

A

Pit invaginates to form coated vesicles
Coated vesicles are actively (aka using ATP) uncoated
They then fuse with endosomes

38
Q

What is the importance of insulin and it’s receptor remaining associated in the endosome?

A

The mechanism allows for a reduction in the number of receptors on the cell surface
This desensitises the cell to constant high circulating insulin

39
Q

What is transcytosis?

A

When ligands remain attached to their receptors and are transported across the cell
Eg maternal immunoglobulins are transferred to the foetus
Eg immunoglobulin A is transported from the circulation to bile in the liver

40
Q

What are the modes of RME?

A

1-Where the receptor is recycled and the ligand degraded
2-Where both the receptor and the ligand are recycled
3-Where both the receptor and the ligand are degraded
4-Where both the receptor and the ligand are transported

41
Q

Give an example and describe the function of a ligand involved in mode 1 of RME

A

Ligand: LDL
Function: metabolic uptake

42
Q

Give an example and describe the function of a ligand involved in mode 2 of RME

A

Ligand: transferrin
Function: Fe3+ uptake

43
Q

Give an example and describe the function of a ligand involved in mode 3 of RME

A

Ligand: Insulin
Function: Metabolic control

43
Q

How do membrane-enveloped viruses and toxins take advantage of RME? Give examples

A

Once in the endosome, the acidic pH allows the viral membrane to fuse with the endosomal membrane, releasing toxins or viral RNA into the cytoplasm
Eg the diphtheria and cholera toxins, both of which bind to the GM1 ganglioside

44
Q

Give an example and describe the function of a ligand involved in mode 4 of RME

A

Ligand: maternal IgG, IgA
Function: transfer of large molecules across a cell

ESA2 (39 decks)

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