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Cell physiology and pharmacology > Lecture 12- GPCRs > Flashcards

Lecture 12- GPCRs Flashcards

1
Q

What is signal transduction?

A

Receptors needed for cells to respond to extracellular signalling molecules (hormones, NT, GF)

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2
Q

receptors can be

A

intramembrane (majority) or intracellular

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3
Q

how many types of GPCR identified in human genome

A

> 800 (>2% of identified genes)

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4
Q

structure of GPCRs

A
  • Single peptide sequence (300-1200 amino acids)
  • 7 transmembrane structures
  • N terminal outside the cell
  • C terminal faces inside the cell
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5
Q

N terminal

A

outside the cell- ligand binding domain

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6
Q

c terminal

A

faces inside the cell- Gprotein

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7
Q

where do ligands bind on GOCR

A

two different sites:

  • binding site on N-terminal region
  • bidding site in transmembrane
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8
Q

each receptor subtype is specific for

A

one chemical ligand

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9
Q

ligand binding activates the receptor which directly or indirectly

A

brings about change in the cellular activity

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10
Q

percentage of prescription drugs that exert their therapeutic effects directly or indirectly at the GPCRs

A

40%

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11
Q

agonists

A

bind and activate

• Leading to intracellular signal transduction

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12
Q

example of a GPCR agonist

A

salbutamol (B adrenoreceptor agonists)

morphine (u-opioid receptor agonist)

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13
Q

antagonists

A

bind and block the effect of agonist on the receptor

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14
Q

example of a GPCR antagonist

A

cardiovascular (hypertension) B-adrenoreceptorsantagonists

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15
Q

what can GPCRs respond to

A

1) Sensory GPCRs- light, odours and taste
2) Ions
3) NT
4) Peptide (glucagon, insulin, adrenaline) and non-peptide hormones
5) Large glycoproteins- TSH

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16
Q

G protein is made up of three different proteins

A

Alpha and Beta/Gamma(single unit)

17
Q

activation of the GPCR facilities activation of G protein on the inside of the membrane..

A
  1. When adrenaline binds the GPCR changes its conformation- initiation of cascade
  2. Conformational change attracts G protein, which is activated
    a. Alpha Part of G-protein bound to GDP
  3. G protein activated- exchanges GDP for GTP
  4. Once GTP is bound to alpha subunit it dissociates from the beta and gamma subunit- leaving a free alpha-GTP and free B/Y subunit which both have effector role
18
Q

Termination of G-protein signalling

A
  1. GTPase hydrolyses the GTP that’s bound to the alpha submit releasing Pi returning alpha to Alpha-GDP state- no effector function
  2. Alpha-GDP ready to be reactivated by GPCR
19
Q

Where is the G protein (Alpha and beta-gamma subunit) found

A

inserted in the cell membrane uses plasma membrane as a monorail to move around in the plane of the membrane

20
Q

types of G protein

A

GalphaS
GalphaI
GalphaQ

21
Q

human genome encodes how many Ga proteins

A

20

22
Q

human genome encodes how many GB proteins

A

5

23
Q

human genome encodes how many GY proteins

A

12+

24
Q

how many Ga-BY combinations

A

over 1000

25
Q

G protein diversity means that

A

an extracellular signal, working via a specific GPCR, will activate a single, or small sub-population of G proteins and effectors in the cell to bring about a specific cellular response.

26
Q

alpha1 receptor

A

Q

  • stimulate phospholipase C
  • increase IP3 and DAG
27
Q

alpha 2 receptor

A

I

  • decrease adenylyl cyclase activity
  • decrease cAMP
28
Q

beta 1 receptor

A

S

  • increase adenylyl cyclase activity
  • increase cAMP
29
Q

beta 2 receptor

A

S

  • increase adenylyl cyclase activity
  • increase cAMP
30
Q

M1 receptor

A

Q

  • stimulate phospholipase C
  • increase IP3 and DAG
31
Q

M2 receptor

A

I

  • decrease adenylyl cyclase activity
  • decrease cAMP
32
Q

M3 receptor

A

Q

  • stimulate phospholipase C
  • increase IP3 and DAG
33
Q

M4 receptor

A

Q

  • stimulate phospholipase C
  • increase IP3 and DAG
34
Q

interfering with G-protein function

A

target the GTPase enzyme

35
Q

which toxins are used to study GPCR-G- protein signaling

A

vibrio cholera

pertussis toxin (Ptx)

36
Q

vibrio cholera

A

covalent modification of αs subunit

 Stops the αs from turning itself off
• Can undergo GDP for GTP exchange
• Can signal
• But cannot turn itself off via GTPase
 Causes sustained αs mediated signal- causing overactivation of adenylyl cylase- increase in [cAMP]
 High [cAMP] opens water channels- releasing water and electrolytes into the lumen of the gut- diarrhea and dehydration

37
Q

Pertussis toxin (hooping cough)

A

o Toxin covalently modifies αi subunit

 Prevents alpha subunit releasing GDP for GTP exchange

Cell physiology and pharmacology (20 decks)

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