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Semester 2 - Membranes and Receptors areen > Session 7 - Signal Transduction in Biological Membranes > Flashcards

Session 7 - Signal Transduction in Biological Membranes Flashcards

1
Q

What are G protein coupled receptors?

A

A family of receptors that act by altering the activity of effectors

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2
Q

What do G-proteins activate in order to interact with effectors?

A

Gunaine nucleotide binding proteins

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3
Q

What is the the word to describe G-proteins?

A

Heterotrimeric

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4
Q

How can G-proteins be described as heterotrimeric?

A

The consist of three different subunits - alpha, beta and gamma

  • Beta and gamma bind tightly together and form single unit
  • Alpha has a GTP binding site which has GTPase activity (slowly hydrolyses bound GTP to GDP)
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5
Q

Where is the G-protein usually present in the cell, and in what form?

A

at the inner face of the plasma membrane

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6
Q

Describe what occurs when G-protein coupled receptor binds an agonist

A

Agonist binds receptor
Protein-Protein interaction releases GDP, binds GTP to alpha subunit
a-GTP and bg released and interact with effectors
GTP hydrolysed to GDP
a-GDP and bg reform heterotrimer

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7
Q

What is the interaction of G proteins with effectors inhibited by?

A

Intrinsic GTPase activity of alpha subunit. Once bound GTP hydrolysed to GDP, the affinity of alpha subunit for bg increases, and the hetertotrimer reforms

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8
Q

How g proteins be thought of a switches and timers?

A

The on switch is receptor-facilitated GDP/GTP exchange

the timer/off switch is governed by the length of time taken for GTP hydrolysis.

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9
Q

What is the role of stimulatory G (Gs) proteins?

A

Plays an intermediate role - stimulate adenylyl cyclase to produce cAMP

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10
Q

What is the role of inhibitory G protein (Gi) paths?

A

Inhibit adenylyl cyclase, reducing cAMP

Also effect ion channels and signalling pathways involved in growth and differntiation

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11
Q

What do Gq proteins interact with?

A

Activate phospholipase C, which hydrolyses PIP2 to IP3

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12
Q

What is the name of the light sensing receptor in the eye, and what does it activate?

A

Rhodopsin, activates Gt whichin turn activates a phosphodiesterase enzyme that hydrolyses cyclic GMP to 5’-GMP

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13
Q

What does adrenaline activate when activating b adrenoreceptors?
Receptor, G protein, effects, physiological response

A

b-Adrenoceptor
Gs
Stimulates Adenylyl Cyclase
Glycogenolysis, lipolysis

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14
Q

What does acetylcholine activate when interacting with M3?

A

Gq
Stimulates Phospholipase C
Smooth Muscle Contraction

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15
Q

What does Ach activate when interacting with M2?

A

Gi
Inhibits Adenylyl Cyclase

Stimulates K+ Channel
Slowing of Cardiac Pacemaker

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16
Q

What does light do?

A

Rhodopsin
Gt
Stimulates Cyclic GMP Phosphodiesterase
Visual Excitation

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17
Q

What G protein and effector do the following use?
a1
a2

A

a1 - Gq, stimulate phospholipase C

a2 - Gi, inhibit adenylyl cyclase

18
Q

What G protein and effector do the following use?
b1
b2

A

b - Gs, stimulate adenylyl cylase

19
Q

What G protein and effector do the following use?
M1
M2
M3

A

M1 + M3 - Gq, stimulate phospholipase C,

M2 - Gi, inhibit adenylyl cyclase

20
Q

How many Ga, Gb and Gg exist?

A

20 Ga, 5Gb and 12+ Gg proteins.

21
Q

How may possible Ga, Gb and Gg combinations are there?

A

over 1,000

22
Q

How many receptor types are there, and what do they interact with?

A

800 receptor types, which can interact with different G subtypes to activate/inhibit 10 or more enzyme/ion channel effectors.

23
Q

What do Cholera (CTx) and Petussis (PTx) toxin do the G protein cycle?

A

enzymes that ADP-Ribosylate specific G-Proteins

24
Q

What does CTx do?

A

Eliminates the GTPase activity of Gsa, leading it to become irreversibly activated (opening chloride ion channels!)

25
Q

What does PTx do?

A

PTx interferes with the GDP/GTP exchange on Gia. This leads Gia to become irreversibly inactivated.

26
Q

What can genetic changes to GPCRs cause?

A

loss-of-function or gain-of-function mutations

27
Q

How is retinitis Pigmentosa caused?

A

By a loss-of-function mutation to Rhodopsin

28
Q

What are the symptoms of retinitis pigmentosa?

A

Severe visual impairment

29
Q

How is nephrogenic diabetes insipidus cause?

A

By a loss-of-function mutation to V2 Vasopressin receptor

30
Q

What are the symptoms of nephrogenic diabetes insipidus?

A

improper response of the kidney to ADH, leading to a decrease in the ability of the kidney to concentrate the urine by removing free water

31
Q

What is Familial Male Precocious Puberty caused by?

A

a gain-of-function mutation (Receptor active without ligand) to the Luteinising Hormone (LH) Receptor

32
Q

What are the symptoms of amilial Male Precocious Puberty?

A

Early onset puberty?

33
Q

Name three diseases caused by mutations to G-protein coupled receptors

A

Retinitis Pigmentosa
Nephrogenic Diabetes Insipidus
Familial Male Precocious Puberty

34
Q

What is the mechanism of adenylyl cyclase?

A

This enzyme hydrolyses cellular ATP to generate cyclic AMP. Cyclic AMP interacts with a specific protein kinase (PKA) which phosphorylates a variety of proteins to affect cell activity

35
Q

What does adenylyl cylcase cause to happen in cells?

A
  • increased Glycogenolysis and gluconeogenesis in the liver
  • increased lipolysis in adipose tissue
  • relaxation of a variety of types of smooth muscle
  • positive inotropic and chronotropic effects in the heart.
36
Q

What is the mechanism of phospholipase C?

A

Activates by Gq and hydrolses PIP2 to IP3

IP3 exerts effects by interacting with receptors on ER to allow calcium to enter cytoplasm

37
Q

How does Cyclic GMP phosphodiesterase work?

A

It regulates the breakdown of the second messenger cyclic GMP phosphodiesterase by Gt

38
Q

How are G-protein coupled receptor pathways deactivated

A
  • When activated, receptor vunerable to variety of protein kinases that phosphorylate the receptor and prevent it activating further G proteins
  • The active lifetime of a GTP may be limited by cellular factors that stimulate intrinsic GTPase activity of Ga subunit
  • Cells contain high activity enzymes that metabolise second messengers, rapidly returning their levels to the basal (favoured state)
  • Enzymatic cascades activated downstream of second messenger/protein kinase activation act to oppose their effect.
39
Q

How is chronotrophy in the heart regulated?

A
  • Rate at which SA node fires affect by Ach release by parasympathetic nerves
  • Activation of M2 receptors increases oen probability of K+ channels via Gi
  • Increasing membrane permeability to K+ causes hperpolarisation, slowing intrinsic firing rate
  • This causs negative chronotrophic effect
40
Q

How is intotrophy in heart regulated?

A
  • Sympathetic innervation of cardiac ventricles can influence force of contraction
  • Activation of B adreno receptors increases open probability of voltage operated calcium channels via Gs
  • Gs both interact directly with VOCCs and indirectly via cyclic AMP –> PKA –> phosphorylation and activation VOCCs
  • Influx of Ca2+ brings about postive inotropic effect
41
Q

How is arteriolart vasoconstriction regulated?

A

Sympathetic release of noradrenaline acts on 1-adrenoceptors to stimulate phospholipase C and IP3 production via Gq.
The IP3 releases ER Ca2+ (See above) and initiates a contractile response.

42
Q

How is neutransmitter release modulated?

A
  • Pre-synaptic G-Protein-Coupled Receptors
  • pre-synaptic u-opiod receptors can be stimulated, either by endogenous opiods or by analgesics such as morphine to couple to GaI proteins.
  • The G subunits liberated from the heterotrimer interact with VOCCs to reduce Ca2+ entry, thus reducing neurotransmitter release.

Semester 2 - Membranes and Receptors areen (15 decks)

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