Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ICPP > GPCRs/Calcium > Flashcards

GPCRs/Calcium Flashcards

1
Q

What is the normal extracellular Ca2+ concentration?

A

1x10-3 M (1mM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the normal intracellular Ca2+ concentration?

A

1x10-7 M (100nm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the normal SER/SR Ca2+ concentration?

A

2-3x10-4 M (200-300 micromoles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What channels cause the influx of Ca2+ into the cytosol from the extracellular fluid? (4)

A

VOCC
Ligand Gated ion Channels
Store operated ion channels

NCX (when cell is heavily depolarised)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What channels cause the efflux of Ca2+ from the cytosol out of the cell?

A

NCX

PMCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which molecules are moved by the NCX? How many of each?

A

3Na+ into the cell

1Ca2+ out of the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What provides the concentration gradient for the movement of Na+ and Ca2+ at the NCX?

A

Concentration gradient set up by the Na/K ATPase pump

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which channels can result in the efflux of Ca2+ from SER/SR stores?

A 
Ryanodine Receptors (RyRs)
IP3 receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What type of GPCRs are activated to produce IP3 that can bind with IP3 receptors?

A

Galpha-q associated GPCRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What acts as the ligand at RyRs? What is the process of efflux of Ca2+ at RyRs called?

A

Calcium ions

Calcium Induced Calcium Release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

In which muscles is contraction driven by CICR?

A

Smooth muscle

Cardiac muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the main driver of Ca2+ release for contraction in skeletal muscle?

A

The T-tubule VOCCs are directly coupled with RyRs, so when VOCCs open, RyRs open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What proteins act to regulate Ca2+ cytosol concentrations and slows down diffusion of the ions within the cytoplasm?

A

Calcium ion buffer proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is an example of a Ca2+ binding protein? Give an example of a protein it interacts with? How many calciums can it bind?

A

Calmodulin
Regulates activity of PMCA
Binds up to 4 calcium ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the 3 superfamilies of cell surface receptor?

A

Kinase linked receptors (receptors with intrinsic enzymatic activity)

Ligand Gated ion Channels

G protein coupled receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give an example of a ligand Gated ion channel. Give an example of a kinase linked receptor. Give an example of a GPCR.

A

Nicotinic ACh receptor

Insulin receptor

Muscarinic ACh receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is affinity?

A

How well a ligand binds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is efficacy?

A

How well a ligand causes a response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is an agonist?

A

Molecule that binds to a receptor and activates it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is an antagonist?

A

Molecule that binds to a receptor and does not activate it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give two examples of B2-adrenoceptor agonists? Which disease are these drugs used in the treatment of?

A

Salbutamol
Salmeterol

Asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Give two examples of u-opioid receptor agonists? What are they used for?

A

Morphine, fentanyl

Analgesia/anaesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Give two examples of b-adrenoceptor antagonists. What are they often used to treat?

A

Propranolol
Atenolol

Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Give two examples of d2-dopamine receptor antagonists. What are they used to treat?

A

Haloperidol
Sulpiride

Schizophrenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

GPCRs can respond to a small variety or great variety of stimuli?

A

A great variety of stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

GPCRs consist of how many polypeptide chains?

A

1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Why are GPCRs sometimes called 7TM receptors?

A

They have 7 transmembrane spanning regions

28
Q

What is the position of the n terminal and c terminal at GPCRs?

A

Extracellular n terminal

Intracellular c terminal

29
Q

What two places at GPCRs do ligands typically bind?

A

At a ligand binding site buried between the TM domains (made up by 2-3 of the domains)

At the n terminal region

30
Q

What are two examples of ligands that bind between the TM domains at GPCRs?

A

Adrenaline

Acetylcholine

31
Q

What are two examples of ligands that bind to GPCRs at the n terminal?

A

Glutamate

Thyroid stimulating hormone

32
Q

What does binding of a ligand do to a GPCR?

A

Causes a conformational change in the GPCR - activating it and allowing it to interact with G proteins

33
Q

What subunits make up a G protein?

A

Alpha

Beta & Gamma (Function together)

Make up a heterotrimer

34
Q

What does interaction of the activated GPCR with the G protein result in?

A

GDP —-> GTP on the alpha subunit of the G protein

Immediate dissociation of the alpha subunit from the beta/gamma subunit

35
Q

Why is GTP able to bind readily to the alpha sub unit once it is activated to?

A

GTP is present at high concentrations in the cell

36
Q

What happens to the two separated units of the G protein to cause a response?

A

They each interact with effector proteins

37
Q

Where in the cell do all the steps of G protein activation, termination etc occur?

A

On the plasma membrane

38
Q

How is G protein signalling terminated?

A

GTP is hydrolysed to GDP

The alpha sub unit possesses GTPase activity and hydrolyses the GTP

High affinity between the two subunits returns, inactive G protein reformed

39
Q

Which G proteins are all beta-adrenoceptors associated with? What is the enzymatic result of their activation?

A

G-alpha-S

Increased adeneylyl cyclase

40
Q

What G proteins are the m4 muscarinic ACh receptors associated with? What is the enzymatic result of their activation?

A

G-alpha-i

Decreased adenylyl cyclase

41
Q

On which GPCRs does pertussis toxin have its effect?

A

Gi GPCRs

42
Q

What effect does Pertussis toxin have on the Gi protein?

A

Causes covalent modification
No GDP/GTP exchange

G proteins can’t be activated

43
Q

What G proteins are affected by cholera toxin?

A

Gs proteins

44
Q

What effect does cholera toxin have on the G protein?

A

Makes the G protein unable to hydrolyse GTP

Permanently activated G protein

45
Q

Which reaction does adenylyl cyclase catalyse?

A

ATP —-> Cyclic AMP

46
Q

Which reaction does phospholipase C catalyse?

A

PIP2—-> IP3 + DAG

47
Q

What reaction does PI3K catalyse?

A

PIP2—-> PIP3

48
Q

What reaction does cGMP phosphodiesterase catalyse?

A

Cyclic GMP —> 5’-GMP

49
Q

What are examples of effectors at the ends of GPCR pathways?

A

Enzymes
Ion channels
VOCCs

50
Q

Why is the cell not deprived of ATP during increased activity of adenylyl cyclase?

A

In reality it is a relatively small side reaction

51
Q

What does cyclic AMP primarily bind to after it has been produced?

A

PKA

52
Q

Name 2 GPCRs other than b-adrenoceptors that are Gs preferring.

A

D1-dopamine receptors

H2-histamine receptors

53
Q

Name two examples of Gi preferring GPCRs other than a2, m2 and m4 receptors.

A

D2-dopamine receptors

u-opioid receptors

54
Q

What is the structure of PKA?

A

Has 4 sub units

2 Regulatory
2 catalytic

55
Q

How does cyclic AMP interact with PKA?

A

Cyclic AMP binds with the regulatory sub units of PKA

Release of catalytic sub units

56
Q

What does PKA do?

A

Phosphorylate different substrates

57
Q

Other than the pumps that exist, how else is the very low intracellular calcium ions concentration maintained?

A

Relative impermeability of the plasma membrane and calcium binding proteins

58
Q

Which GPCRs result in increased phospholipase C activation?

A

Gq preferring GPCRs

59
Q

What substrate does phospholipase C work on?

A

PIP2

Cleaves it to form IP3 and DAG

60
Q

What does increased DAG production result in?

A

Activation of PKC

61
Q

The activation of IP3 receptors can increase intracellular calcium ion concentration how many fold within a few seconds?

A

5-10 fold

62
Q

Other than a1, m1 and m3 receptors, name a receptor that prefers Gq proteins?

A

H1-histamine receptors

63
Q

Increased intropy is the result of activation of which receptors? How does it cause increased force of contraction?

A

B1-adrenoreceptors

PKA phosphorylates VOCCs, increased calcium —> increased contraction

64
Q

Vascular smooth muscle contraction (vasoconstriction) is controlled by which GPCR?

A

a1-adrenoceptors

65
Q

Bronchoconstriction can be affected by which GPCR?

A

M3-muscarinic receptors

66
Q

What is an example of an effector molecule for the activated beta/gamma subunit?

A

VOCCs

67
Q

What effect can beta/gamma sub units have at VOCCs at synapses?

A

Inhibit specific VOCCs reducing calcium influx, reducing neurotransmitter release

ICPP (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions