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BIOC2003 > Signalling 1 > Flashcards

Signalling 1 Flashcards

1
Q

How is signal transduction specific?

A
  1. Horomone released into local area
  2. Each cell expressed specific group of receptors - different receptors can bind same horomone but stimulate production of different secondary messengers
  3. Secondary messenger has specific effects
  4. Cells express different isoforms of effectors
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2
Q

How is signal transduction sensitive?

A

Hormone receptors have high affinity for their hormone so only low concentrations needed.
-> Enzyme catalysing formation of secondary messenger is a point of amplification
-> Some effectors stimulated, some inhibited + so enzymes favouring one pathway are activated while the opposing pathway is shut down
=> metabolism is turned around

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3
Q

Outline receptor desensitisation

A
  1. Enzyme shuts down signal when hormone not present
  2. Enzyme breaks down 2nd messenger
  3. Enzyme acts in opposition to 2nd messenger action
  4. Pathway is no longer stimulated, despite presence of hormone
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4
Q

How do signalling pathways integrate?

A
  1. Cells express multiple hormone receptors on cell surface + can be exposed to many different hormones simultaneously
  2. Each diff. receptor can bind its respective hormone at same time as other receptors
  3. Different receptors may modulate concentrations of same sex. messengers
  4. Different signalling pathways may alter same effectors
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5
Q

Receptor: Hormone allosteric effects

A

Cytosolic domain

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6
Q

Ca++ calmodium allosteric effects

A

Exposes hydrophobic areas that allow calmodium to interact with other proteins

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7
Q

cAMP:PKA(R) allosteric effects

A

Regulatory subunits dissociate activating catalytic subunits

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8
Q

Enzyme that acts opposite to Phosphatase and requirements

A

Kinase , ATP

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9
Q

What bonds can phosphoryl group form?

A

H bonds

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10
Q

Why do kinase act as amplification points?

A

Each kinase can phosphorylate multiple target proteins

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11
Q

Protein domains are

A

reoccuring with high affinity for certain types of sequences

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12
Q

Phosphotyrosine binding domain and SH2 similarities

A

Tyr- P

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13
Q

SH3 binding domain consists of

A

3 prolines

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14
Q

PH binding domain consists of

A

P-Inositol -P P

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15
Q

EF-hand binding domain consists of

A

Ca++

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16
Q

A paracrine hormone

A

Acts on nearby cells

17
Q

Prostaglandins belong in what class of hormone?

A

Eicosanoids

18
Q

Which GPCR loop interacts with G proteins?

A

3/4 or 5/6

19
Q

How many isoforms of Ga, Gb and Gy

A

20, 5, 6

20
Q

Gt classification

A

Activates retinal cyclic GMP phosphodiesterase

21
Q

Outline Gs stimulation by adrenaline

A
  1. Gsa activation, GDP -> GTP
  2. Gsa dissociation from b and y -> activates AC
  3. ATP -> cAMP
  4. cAMP activation of PKA by 4x attachment to R sub-units
  5. R sub-units dissociate from catalytic sub-units
  6. Target protein phosphorylated by PKA
22
Q

PKA characteristics

A

R2C2 heterotetramer: serine/ threonine kinase

  • phosphorylates several enzymes
  • > lipase, aCoA carboxylase, glycogen synthase, TF CREB +
23
Q

PKA consensus sequence

A

Arg, Arg, X, Ser/Thr, Z

24
Q

PKA sub-unit regulatory sequence

A

Arg, Arg, Gly, Ala, Ile

25
Q

Adrenaline: Gs points of amplification

A
  1. Adrenaline: receptor complex catalyses GDP:GTP on multiple G-proteins -> each Ga binds to 1 AC
  2. Each AC can catalyse formation of many cAMP
    - > 4 cAMP per 2x PKA
  3. Each active PKA can phosphorylate many proteins
26
Q

Shutting down of Adrenaline: receptor complex

A
  1. Adrenaline no longer present GTP -> GDP
  2. GDP + a -> a + by subunits
  3. AC no longer active
  4. Remaining cAMP converted to AMP by cyclic nucleotide PDE
  5. R-subunits no longer occupied by cAMP so reform with catalytic subunits
  6. Phosphatases dephosphorylate proteins
27
Q

How do arrestins mediate desensitisation?

A
  1. Block cytoplasmic face of receptor which prevents G-protein binding + activation
  2. Arrestin links receptor to clathrin + AP2 -> endosome to form lysosome or recycled
28
Q

How does beta ARK mediate desensitisation?

A

βARK,a serine/threonine kinase, will phosphorylate serine and threonine residues on the β-adrenergic receptor.
-> This will facilitate Beta-arrestin’s binding to the receptor. Additional stimulation by epinephrine will now be unable to activate Gs due to arrestin.

29
Q

How is beta ARK an example of negative feedback?

A

It’s activated by phosportylation of serine/ threoinine residues from PKA -> prevents overstimulation of of b-adrenergic receptor

BIOC2003 (13 decks)

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