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ESA 2 > Signal Transduction > Flashcards

Signal Transduction Flashcards

1
Q

Give an agonist of beta-2 adrenoceptors.

A

Anti-asthma
Salbutamol
Salmetenol

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2
Q

Give an agonist of a mu-opioid receptor.

A

Analgesic
Morphine
Fentanyl

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3
Q

Give an antagonist of beta adrenoceptors

A

Hypertension treatments
Propanolol
Atenolol

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4
Q

Give an antagonist of D2 dopamine receptors

A

Neuroleptics e.g. anti-schizophrenics
Haloperidol
Sulpinide

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5
Q

What mutation gives rise to nephrogenic diabetes insipidus?

A

Loss of function mutation to V2 vasopressin receptor

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6
Q

Describe the general structure of GPCR proteins.

A

One polypeptide chain
7 transmembrane domains
Extracellular N terminus
Intracellular C terminus

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7
Q

Where can ligands bind to a GPCR?

A

Between the transmembrane domains or on a specialised N-terminus

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8
Q

What governs the magnitude of the signal passed on from a GPCR?

A

A timer system in the GPCR

Cellular regulation of GTPase

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9
Q

What G-protein alpha subunit is associated with a beta-adrenoceptor?

A

Gs

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10
Q

What G-protein alpha subunit is associated with an alpha-2 adrenoceptor?

A

Gi

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11
Q

What G-protein alpha subunit is associated with an alpha-1 adrenoceptor?

A

Gq

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12
Q

What G-protein alpha subunit is associated with the M2 and M4 muscarinic receptors?

A

Gi

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13
Q

What G-protein alpha subunit is associated with the M1 and M3 muscarinic receptors?

A

Gq

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14
Q

How does cholera toxin affect G-proteins?

A

Eliminates GTPase activity on Gs-alpha which makes it irreversibly activated

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15
Q

How does pertussin toxin affect G-proteins?

A

Interferes with GDP/GTP exchange on Gi-alpha so it becomes irreversibly activated

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16
Q

What is the function of adenylyl cyclase?

A

ATP to cAMP

17
Q

What is the function of phospholipase C?

A

PIP2 to IP3 and DAG

18
Q

What is the function of phosphoinositide-3-kinase (PI3K)

A

PIP2 to PIP3 (thought to be a survival signal)

19
Q

What is the function of cGMP phosphodiesterase?

A

cGMP to 5’GMP

20
Q

Give two effectors linked to G-proteins which are ion channels.

A

Voltage-operated calcium channels (VOCC)

G-protein regulated inwardly-rectifying K+ channels (GIRKs)

21
Q

Give an example of a Gs coupled receptor

A

Beta adrenoceptors
D1 dopamine receptors
H2 histamine receptors

22
Q

Give an example of a Gi coupled receptor

A

Alpha-2 adrenoceptors
D2 dopamine receptors
Mu-2 opioid receptors

23
Q

What enzyme does cAMP exert the majority of it’s action on and how?

A

Protein kinase A
cAMP binds the regulatory subunits which sit in the enzyme site, allowing the catalytic subunits to dissociate, allowing full activity.

24
Q

What effect does activation of an Gq coupled receptor have on a cell?

A

Activates phospholipase c which cleaves PIP2 to DAG (in the membrane) and IP3 (in the cell)
IP3 then activates IP3 receptors in the ER which are calcium channels, increasing the release of calcium.
DAG and the extra calcium activate protein kinase C which has it’s own specific intracellular targets.

25
Q

Give an example of a Gq coupled receptor

A

Alpha-1 adrenoceptors
M1 muscarinic receptors
H1 histamine receptors

26
Q

Where does the most significant signal amplification begin to happen?

A

After enzyme activation

27
Q

Describe how activation of specific GPCRs in the heart causes positive ionotropy.

A

Adrenaline or noradrenaline activate B1 adrenoceptors. This allows cAMP formation by adenylyl cyclase.
cAMP activates PKA which phosphorylates targets, one of which is VOCC in the membrane.
This increases calcium concentration in the cell and therefore contractility.

28
Q

Describe how vasoconstriction is initiated by noradrenaline.

A

Interacts with alpha-1 adrenoceptors which increases calcium concentration and protein kinase C activity by Galpha q.
This causes increased contractility

29
Q

Describe how acetylcholine can cause bronchoconstriction.

A

ACh binds to M3 muscarinic receptors.

30
Q

How is neurotransmitter release modulated, using the example of morphine?

A

Morpine activates a mu-opioid receptor, which allows the dissociation of the beta-gamma subunit.
This inhibits N-type VOCC, reducing calcium influx and therefore lowering neurotransmitter release.
This is modulating rather than inhibiting.

31
Q

Why is cell context important when discussing the action of GCPRs?

A

There is cell background specificity as the cellular components determine the exact effects, but in a specific cell the changes on activation will be hard-wired.

ESA 2 (46 decks)

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