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GMC > Cell signalling 2(?) > Flashcards

Cell signalling 2(?) Flashcards

1
Q

LOs:

A
  • A basic understanding of how monomeric G-proteins are activated & inactivated using GEFs & GAPs
  • Structure of trimeric G proteins and of G-protein coupled receptors
  • Activation of a GPCR & how this activates a trimeric G protein
  • Examples of 2nd messengers & how cAMP is produced
  • The effect of cAMP of PKA
  • Basic structures of RTKs
  • How RTKs are activated & are able to activate signal transduction pathways
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2
Q

What binds to G-protein coupled receptors initially?

A

Ligand (first messenger)

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3
Q

What happens to G-protein coupled receptors when ligand binds to it?

A

Activates an intracellular G-protein which in turn activates an enzyme which changes the conc of an intracellular second messenger (small molecule e.g. cAMP)

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4
Q

What is the structure of a G-protein coupled receptor?

A
  • 7 transmembrane alpha helical regions
  • 4 extracellular regions (on the outside of the cell between alpha regions)
  • 4 cytosolic regions (loop into cell, same as above)
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5
Q

What are 4 examples of stimuli (ligands) in GPCR systems?

A
  • Adrenaline
  • Light
  • fMet peptide
  • ACh
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6
Q

For adrenaline (as a GPCR stimulus) name the:
Receptor, effector, 2nd messenger & response in the system:

A

Stimulus = adrenaline

Receptor = beta-adrenergic

Effector = adenylate cyclase

2nd messenger = cAMP

Response = glycogen breakdown

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7
Q

For light (as a GPCR stimulus) name the:
Receptor, effector, 2nd messenger & response in the system:

A

Stimulus = light

Receptor = rhodopsin

Effector = cGMP phosphodiesterase

2nd messenger = cGMP

Response = photo-reception

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8
Q

For fMet peptide (as a GPCR stimulus) name the:
Receptor, effector, 2nd messenger & response in the system:

A

Stimulus = fMet peptide

Receptor = chemotactic receptor

Effector = phospholipase C

2nd messenger =IP3 (Ca2+) & DAG

Response = chemotaxis

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9
Q

For ACh (as a GPCR stimulus) name the:
Receptor, effector, 2nd messenger & response in the system:

A

Stimulus = ACh

Receptor = muscarinic ACH receptor

Effector = K+ channel

2nd messenger = K+

Response = slowing pacemaker activity

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10
Q

What state are G-protein receptors in when GDP is bound?

A

“Inactive” - the system is considered off

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11
Q

What state are G-protein receptors in when GTP is bound?

A

“Active” - the system has been switched on

The active G-protein has intrinsic GTPase activity

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12
Q

What are the 2 types of GTP-binding proteins?

A
  • Monometric
  • Trimetric
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13
Q

How G-proteins regulate how fast they act?

A

By how quickly they switch out GDP for GTP

GTP activates the receptor - therefore the faster it is switched in the more the receptor will react

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14
Q

What are GAPs and what do they do?

A

GTPase activating proteins

Inactivate the G protein by stimulating hydrolysis of GTP to GDP

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15
Q

What are GEFs and what do they do?

A

Guanine nucleotide exchange factors (GEFs)

Activate the G protein by stimulating it to release GDP

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16
Q

What is the trimeric structure of G proteins?

A

3 subunits:

Alpha, beta & gamma

17
Q

How are the beta & gamma subunits in a G-protein arranged?

A

Beta & gamma are very tightly bound

18
Q

What is the role of the beta and gamma unit?

A

To encourage the breakdown of GTP to GDP

19
Q

Where are G-proteins attached to?

A

The cytoplasmic face of the plasma membrane

20
Q

Describe the process of G protein relay signals:

A
  • G protein attached to cytoplasmic face of the plasma membrane
  • Alpha & beta subunits have covalently attached lipid molecules that aid binding to the plasma membrane
  • Activation of G protein, via receptor activation
  • Inactivation of G protein by GTP hydrolysis by alpha-subunit

(beta-gamma complex may dissociate)

21
Q

What is the process of G protein receptors creating a second messenger system?

A
  • Binding of ligand to GPCR changes the conformation of the receptor
  • Allows GDP to be exhanged for GTP (acts as a GEF)
  • alpha & beta-gamma subunits may dissociate (but not always)
  • Activated G protein elicits a second messenger system
22
Q

What are DAG and IP3 derived from?

A

A lipid

23
Q

What does DAG generally do?

A

Floats around & stimulates protein kinase C

24
Q

What does IP3 generally do?

A

Diffuse thru cytosol & reach endoplasmic reticulum, will allow calcium to diffuse into the cell

25
Q

What is cAMP produced from?

A

Produced from ATP by adenylyl (adenylate) cyclase, releaseing pyrophosphotase

cAMP conc is kept low

26
Q

What do phosphodiesterases do?

A

Cleave cAMP to 5’ AMP

Breaks down cAMP

27
Q

Look at the diagram for activation of adenylyl cyclase by trimeric G protein :)

A

COol

28
Q

What is the effect of cAMP?

A
  • Activate cAMP-dependent protein kinases (PKA)
  • PKA exists in inactive form but binding of cAMP causes dissociation of regulatory subunits
29
Q

How is protein kinase A broken down?

A

PKA has 4 subunits - 2 are regulatory cAMP removes these 2 & allows active areas to go off

Protein kinase 2, the A kinase acts w A kinase anchoring proteins, gets locked onto these so it will do the jobs it’s required to do

30
Q

What is the effect of activated PKA?

A

Ligand arrives, leads to adenylyl cyclase activated - using ATP cAMP is activated & stimulates various other molecules

Some genes known to respond when cAMP is present, these ones have CREb transcription factors

31
Q

What are the actions of activated PKA?

A
  • PKA can phosphorylate target proteins e.g. metabolic enzymes in glycogen metabolism
  • Alter gene transcription cia cAMP response element binding protein (CREB)
32
Q

What does RTKs stand for?

A

Receptor Tyrosine Kinases

33
Q

Go from RTKs

A

hahfnvw

GMC (6 decks)

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