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IMS > Intracellular signalling > Flashcards

Intracellular signalling Flashcards

1
Q

What is signal transduction

A

Converting 1st messenger to cellular function

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2
Q

What are the stages of intracellular signalling

A
  • reception
  • signal transduction
  • cellular response
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3
Q

What is the hierarchy in intracellular Signalling

A
  • 1st messenger
  • receptor
  • G-protein
  • effector enzyme
  • 2nd messenger
  • protein kinase
  • target protein
  • cell response
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4
Q

What is amplification

A
  • 1st messenger —> large response
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5
Q

What is cross-talk in specificity

A
  • 1st messenger stimulating diff. responses in diff cells
  • 1st messenger bind to diff receptors on same cell
  • 1st messenger stimulate different pathway
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6
Q

Example of specificity

A
  • adrenaline
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7
Q

Why is there complexity in signal transduction

A
  • 1000+ GPCRs
  • 500+ protein kinases
  • cross-talk
  • cell-type specificity
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8
Q

What are G-proteins

A
  • guanine nucleotide binding proteins
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9
Q

What is GTP

A

Guanosine trisphosphate

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10
Q

What is GDP

A

Guanosine diphosphate

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11
Q

What is the function of GTP

A
  • high energy

- activate G-protein

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12
Q

What do G-proteins do as GTPases

What do ligand-receptors do

A

Hydrolyse GTP —> GDP
Energy released
Opposite to GTPases

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13
Q

What is the process of receptor associated G-proteins

A
  • ligand binding —> GDP/GTP exchange
  • effector activation —> 2nd messenger
  • hydrolysis of GTP —> GDP
  • re-association of G protein subunits
  • loss of 2nd messenger
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14
Q

What is the effector enzyme and 2nd messenger of the following G-proteins:

  • Gas
  • Gai
  • Gag
A
  • adenylate cyclase (stimulation), cAMP
  • adenylate cyclase (inhibition), cAMP
  • phospholipase C (stimulation), DAG
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15
Q

What is the mechanism of cholera toxin (Gs)

A
  • inhibits GTPase activity
  • GTP remains “on”
  • over-stimulation of adenylate cyclase
  • accumulation of cAMP
  • loss of Cl-
  • osmotic gradient
  • water loss
  • dehydration
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16
Q

What are the syndrome of whooping cough

A
  • paroxysmal cough

- whooping

17
Q

What is the prevalence of whooping cough

A
  • 40-50m cases/y

- >250000 death/y

18
Q

What is the cause of whooping cough

A
  • bordetella pertussis
  • airborne respiratory droplet
  • virulent factor: pertussis toxin
19
Q

What is the treatment & prevention of whooping cough

A
  • antibiotics

- vaccination

20
Q

What is the mechanism of pertussis toxin (Gi)

A
  • prevents GDP/GTP exchange by Gi
  • “off” position
  • accumulation of cAMP
  • insulin secretion
  • increased sensitivity to histamines
21
Q

What is a 2nd messenger

A
  • short-acting intracellular molecule
  • rapidly formed/ released
  • result of receptor activation
22
Q

What are the 5 most common 2nd messengers

A
  • cyclic AMP, cAMP
  • cyclic GMP, cGMP
  • diacylglycerol, DAG
  • inositol 1,4,5-trisphosphate, IP3
  • intracellular calcium, Ca2+
23
Q

What is the production of cGMP catalysed by

A
  • guanylate cyclase

- activated by NO

24
Q

What enzyme breaks down cGMP

A
  • PDE

- GMP formed

25
Q

The activation of which G-protein causes the production of DAG, IP3 and Ca2+

A

Gq

26
Q

Give examples of receptors activating Gq pathway

A
  • angiotensin ii on AT1 receptor

- adrenaline on alpha 1-adrenegeric receptor

27
Q

What is the mechanism for Gq activation

A
  • ligand-binding —> GDP/GTP exchange
  • effector enzyme activated —> 2nd messenger produced
  • IP3 released in cytosol —> Ca2+ released
  • DAG remains in memb. —> kinase C activated
28
Q

What binds to ER to trigger Ca2+ release

A
  • IP3
29
Q

What are protein kinases

A
  • enzymes facilitate transfer of P from ATP to specific aa (Ser, Thr, Tyr) in specific protein
30
Q

What are the 3 main kinases groups

A

Serine/threonine
Tyrosine kinases
Dual-specificity (MAP –>MKKs)

31
Q

How can kinases modulate protein function

A
  • phosphorylation —> conformational change in protein

- phosphorylation of transcription factor

32
Q

Check out slide 63 on lecture

A

Also check revision tip at bottom

33
Q

What diseases are kinases inhibitors used to treat

A
  • cancer
  • cardiovascular disease
  • HIV
  • AD
34
Q

What are G proteins

A
  • heterotrimeric

- Gas, Gai, Gay

35
Q

What are small GTPases

A
  • monomeric

- Ras, Rho

36
Q

Which two G-proteins have the opposite effect on cAMP

A

Gs, Gi

37
Q

what is the production of cAMP catalysed by

A

Adenylate cyclase

38
Q

what is the production of cGMP catalysed by

A

Guanylate cyclase

39
Q

what do PDEs do

A
  • break down cAMP, cGMP

- inhibit caffeine & viagra

IMS (18 decks)

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