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adv mol cell > GPCRs > Flashcards

GPCRs Flashcards

1
Q

how many transmembrane domains do GPCRs have?

A

7 a helices

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2
Q

which TM domain sits next to binding pocket of gpcrs?

A

TM3 centrally located next to binding pocket, crucial for ‘transduction’ of ligand binding

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3
Q

important GPCR structures for binding

A

TM3
extracellular N terminus
other TMs

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4
Q

when is a GPCR activated

A

when a ligand is bound

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5
Q

how are GPCR classes distinguished

A

by structural features of the extracellular domains defining the ‘ligand’ binding site

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6
Q

how are protease-activated receptors activated in platelets

A
  • N terminus is cleaved and acts as ligand to activate itself
  • causes activation of platelets -> bind to exposed collagen
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7
Q

what are G proteins

A
  • Guanine nucleotide-binding proteins
  • GTPase family
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8
Q

G proteins function and regulation

A
  • molecular switches inside cell to transmit signals from extracellular
    stimuli
  • Regulated by ability to bind and hydrolyse GTP (‘on’) to GDP (‘off’)
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9
Q

G proteins structure

A

heterotrimeric complexes made up of ⍺, β, and 𝛾 subunits

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10
Q

mechanism of action of GPCRs

A

Inactive state – GDP bound to the alpha subunit
1. Ligand binding = conformational change in receptor that activates G-protein
2. GDP released and ⍺ subunit separates from other subunits and binds GTP – now active
3. Binds to target protein in membrane to elicit a response within the cell

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11
Q

how are GPCRs controlled

A
  • act as timers
  • Duration of signalling by activated trimeric G protein is regulated by rate of GDP hydrolysis by Gα
  • RGS proteins stimulate GTPase activity in the ⍺ subunit
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12
Q

GiαGPCR function

A
  • a-adrenergic R
  • negative feedback in neuronal synapses
  • decrease insulin from pancreas
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13
Q

Gqα GPCR function

A
  • a-adrenergic
  • smooth muscle contraction
  • vasoconstriction
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14
Q

Gsα GPCR function

A

β-Adrenergic
β1- increase heart rate
β2 - smooth muscle relaxation

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15
Q

Gtα GPCR function

A

Rhodopsin
Vision

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16
Q

G13a function

A

platelet activation

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17
Q

Golfa GPCR function

A

sense of smell
- specific subunit and cell type determines response using same signalling as other cell types

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18
Q

how do effectors work

A

include enzymes that create 2nd messengers and ion channels whose gating is regulated either directly (β𝛾 subunits) or indirectly by 2nd messengers and their effectors

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19
Q

how does direct activation of an ion-channel occur

A
  • Similar mechanism as ligand-gated channels
  • Slow to open or close
  • Stay open or closed for longer - minutes rather than milliseconds
20
Q

How do activated G proteins regulate the activities of enzymes that control the levels of second messengers

A
  • Second messengers are small molecules that carry signals inside cells
  • e.g Hydrophobic lipids confined to the membrane in which they are generated
  • Small soluble molecules that diffuse through the cytoplasm (cAMP, cGMP)
  • Calcium ions
21
Q

example of melanoma link to GPCR mutation

A

most uveal melanoma have mutations in Gq subunit -> blocking of GTP hydrolysis so subunits are always active -> permanent signal transduction -> growth

22
Q

what factors contribute to the diversity of receptors

A
  • Specificity of the ligand-binding domain
  • the G protein α subunit
  • the effector within a particular cell type
23
Q

how come organisms can respond to different environmental stimuli

A

GPCR diversity

24
Q

how are the effect of a ‘stimulus’ on cell function determined

A

by the receptor and signalling molecules expressed in that cell

25
Q

advantage of determining effect of stimulus on cell function using GPCR knowledge

A

Allows us to specifically target certain receptors for therapeutic gain

26
Q

advantage of determining effect of stimulus on cell function using GPCR knowledge

A

Allows us to specifically target certain receptors for therapeutic gain

27
Q

what are effectors and examples

A

Effectors of trimeric G proteins include enzymes that create 2nd messengers and ion channels whose gating is regulated either directly (βγ subunits) or indirectly by 2nd messengers and their effectors

28
Q

what are second messengers

A

⇒ small molecules that carry signals inside cells
Activated G proteins regulate the activities of enzymes that control the levels of second messengers

29
Q

cAMP second messenger system

A

10 isoforms of receptor - Activated by G⍺s, inhibited by G⍺i
1. Ligand binds to receptor activating G protein
2. α subunit moves and binds to adenylate cyclase in the membrane
3. activated enzyme catalyses formation of a cAMP from ATP
4. cAMP (2nd messenger) activates Protein kinase A
5. PKA phosphorylates/activates protein
6. Initiates a response within the cell

30
Q

isoforms

A

forms of a protein produced by different genes/ same gene but alternative splicing

31
Q

β2 Adrenoceptor regulation of metabolism in liver and skeletal muscle - how does it work?

A

Binding of single Epinephrine molecule to a receptor sets off a signalling cascade resulting in the phosphorylation/activation of enzymes controlling glycogen metabolism

32
Q

4 ways to switch off GPCR signalling

A
  1. Agonist dissociating from receptor
  2. GTPase activity of Gαs
  3. cAMP breakdown by phosphodiesterase
  4. Dephosphorylation of enzymes
33
Q

difference between cAMP and cGMP second messenger signalling

A

in cGMP
- Enzyme is guanylate cyclase which can be receptor bound or ‘free’ in the cytoplasm
- Converts GTP to 3’, 5’-cyclic guanosine monophosphate (cGMP)

34
Q

how are second messengers encoded

A

conc
fequency of changes in conc

35
Q

what determines local conc of 2nd messengers

A
  • production
  • diffusion
  • removal
  • site of production
36
Q

what is production of cAMP regulated by

A

adenylyl cyclase

37
Q

what is breakdown of cAMP regulated by

A

phosphodiesterase

38
Q

how can effector ion channels be regulated

A

directly (βγ subunits) or indirectly by 2nd messengers and their effectors

39
Q

phospholipase CB function

A

→ cleaves lipids in membrane

40
Q

2nd messengers generated by receptor regulated lipase

A
  1. water soluble and diffuse through cytoplasm e.g IP3 → IP3 receptor (Ca channel)
  2. hydrophobic molecules that remain in membrane e.g DAG → PKC
41
Q

IP3 main functions

A

main functions are to mobilize Ca2+ from storage organelles and to regulate cell proliferation and other cellular reactions that require free calcium

42
Q

lipid kinases function

A

add phosphate groups to lipids

43
Q

purpose of having different isoforms of PLC and PLK

A
  • activated by differnt molecules
  • expressed in different tissues
  • difference in regulatory domains
44
Q

protein kinase C structural/functional features

A
  • PKCs (protein kinase C) are Ser/Thr kinases
  • activated by DAG (C1 domain), and Ca2+ (C2 domain)
  • allows binding to lipids in membrane
  • carboxyl group -> alpha unit binds
45
Q

where on PKC does alpha unit bind

A

carboxyl group

46
Q

where do b/g subunits bind

A

pH unit

47
Q

PKC activation via DAG

A

DAG binding → dissociation of intramolecular pseudosubstrate domain from active site = opens binding site for target protein

adv mol cell (15 decks)

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