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Signal Transduction > Signal Transduction > Flashcards

Signal Transduction Flashcards

1
Q

By which method of action can an agonist cause a conformational change in a receptor?

A

Lock & Key and Curvy grip

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2
Q

Is competitive inhibition action altered by concentration of agonist

A

Yes, the agonist and competitive inhibitor compete to bind to the same site

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3
Q

Is non-competitive inhibition action altered by concentration of agonist?

A

No, they bind to different sites; the non-competitive ligand binds to the allosteric site

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4
Q

How quickly do ionotropic receptors produce a result?

A

milliseconds

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5
Q

How quickly do metabotropic receptors produce a result?

A

seconds

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6
Q

How quickly do kinase linked and nuclear receptors produce a result?

A

hours

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7
Q

When receptors are turned on, what happens to the receptor itself, soon after?

A

the receptors are set to turn themselves off or inhibit themselves through a variety of mechanisms

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8
Q

In a ligand channel, what does the ligand bind to?

A

the binding domain

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9
Q

What is the binding domain of the receptor linked to?

A

A transmembrane pore

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10
Q

What happens to the transmembrane pore when the binding domain is activated?

A

It un-kinks and opens the pore allowing ion passage

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11
Q

Cys-loop receptors are ligand channels, what does their name derive from?

A

The highly conserved cysteine di-sulphide bond in the pore domain

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12
Q

Which subunit is the binding domain found on?

A

Alpha

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13
Q

Which subunit is the pore domain found on?

A

Delta

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14
Q

Name two examples of cys-loop ligand channels

A

Nicotinic (for ACh) and GABAa receptor

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15
Q

Name a GPCR

A

Rhodopsin

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16
Q

What are the three main domains of rhodopsin?

A

transmembrane, extracellular and intracellular

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17
Q

Which domain regulates the g-protein?

A

intracellular

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18
Q

How does a G-protein become activated?

A

by converting GDP to GTP

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19
Q

How do g-proteins self-deactivate?

A

GTPase converts GTP to GDP

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20
Q

The release of GDP causes what to happen?

A

Beta-gamma and delta domain to dissociate

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21
Q

Name 4 targets for delta domain once it has dissociated

A

RhoGEF, Phospholipase C, Adenylyl Cyclase and ion channels

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22
Q

How many transmembrane domains are there in the rhodopsin class of gpcr?

A

7

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23
Q

On which loop is the intracellular domain found?

A

third

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24
Q

When does GPCR desensitisation occur?

A

Often just after the ligand has bound to it

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25
Q

What is heterologous GPCR desensitisation?

A

PKC and PKA inhibit g protein coupling

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26
Q

What is homologous GPCR desensitisation?

A

GRK phosphorylates the receptor causing the inhibition of G-alpha and facilitates Beta-arrestin

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27
Q

What is the action of beta-arrestin

A

to facilitate endocytosis of receptors and initiate recycling back to the membrane

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28
Q

What is the secondary function of beta-arrestin

A

As a signal transducer intracellularly

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29
Q

Are second messengers generally hydrophilic or hydrophobic?

A

hydrophobic

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30
Q

What does 2nd messenger G-alpha S increase?

A

cAMP

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31
Q

What does 2nd messenger G-alpha I decrease?

A

cAMP

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32
Q

Which receptors can release G-alpha S?

A

Beta Adreno, prostacyclin and prostaglandin E2

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33
Q

Which receptors can release G-alpha I?

A

Alpha 2 Adreno, chemokine and cannabinoids

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34
Q

What is a target of amplification?

A

Protein Kinase A (PKA)

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35
Q

Which toxin can activate G-alpha S?

A

Cholera

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36
Q

Which toxin can inhibit G-alpha I?

A

Pertussis

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37
Q

What do G-alpha S/I directly target?

A

Adenylyl Cyclase

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38
Q

What does adenylyl cyclase (AC) catalyse?

A

ATP conversion to cAMP

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39
Q

What does Phosphodiesterase (PDE) do to cAMP?

A

Degrades it to 5’ AMP

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40
Q

How do types of PDE and AC differ?

A

Sequence, regulation, distribution and substrate specificity

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41
Q

cAMP can activate PKA, what can PKA do?

A

Inhibit cAMP

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42
Q

After activation, how long should you wait to see the maximum concentration of cAMP before it is self-inhibited?

A

2-10 minutes

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43
Q

What can Beta 2 (Adreno) linked cAMP rise cause?

A

Increased metabolism and glycogen

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44
Q

What can Beta 1 (Adreno) linked cAMP rise cause?

A

increased calcium channel activity in the heart

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45
Q

Prostacyclin IP and Beta 2 linked cAMP rise cause?

A

Phosphorylation of MCLK (smooth muscle relaxation)

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46
Q

What can Alpha 2 (Adreno) linked cAMP fall cause?

A

Inhibition of NT and insulin release and vascular contraction

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47
Q

What other effects of a fall in cAMP can occur?

A

K+ channels opening and cell hyperpolarisation

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48
Q

What are 3 main examples of G alpha Q receptors?

A

Muscarinic, Angiotensin and Alpha 1 Adreno

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49
Q

When activated, Phospholipase C (PLC) activates what?

A

PIP2

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50
Q

What does PIP2 activate?

A

IP3 and DAG

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51
Q

Can IP3 and DAG diffuse throughout the cell?

A

IP3 can but DAG is membrane bound

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52
Q

What does IP3 cause?

A

Release of intracellular Calcium

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53
Q

What does DAG cause?

A

Activation of Protein Kinase C (PKC)

54
Q

After it has caused the release of Ca2+, what happens to IP3?

A

Phosphorylated to IP

55
Q

After it has activated PKC, what happens to DAG?

A

Kinased to PA

56
Q

What do IP and PA do?

A

Inhibit PIP2

57
Q

What does an intracellular increase of Ca2+ cause?

A

migration of PKC to the membrane to be activated by DAG

58
Q

What are 3 main examples of RhoGEF receptors?

A

Sphingosine 1-phosphate, lysophosphatidic acid and proteinase activted

59
Q

What do RhoGEF do?

A

Facilitate GD/TP exchange at RhoA, activating ROCK

60
Q

What can increased RhoGEF activity result in?

A

Smooth contraction, proliferation, angiogenesis and migration

61
Q

What is the in Vivo half-life of NO?

A

2-5s

62
Q

What does Nitric Oxide Synthase do?

A

Catalyses synthesis of NO

63
Q

What is used up in the formation of NO?

A

L-arginine and O2

64
Q

What is the rate-limiting step in NO synthesis?

A

NOS

65
Q

Which forms of NOS are expressed constitutively?

A

Endothelial (eNOS) and Neuronal (nNOS)

66
Q

Which form of NOS is not expressed constitutively?

A

Inducible (iNOS)

67
Q

Which type of NOS produces more NO?

A

iNOS produces 1000x more

68
Q

What does high blood pressure stress on endothelial cells cause?

A

AKT activation

69
Q

What does AKT do?

A

Stimulate eNOS

70
Q

Which receptor is involved in increasing Ca-Calmodulin?

A

Muscarinic

71
Q

Which receptor is involved in increasing cAMP?

A

Beta Adenergic

72
Q

What can increased PKA and Ca-Calmodulin cause?

A

eNOS stimulation

73
Q

In neuronal tissues, what increases intracellular calcium?

A

Neurotransmitters

74
Q

What does a neuronal increase of Ca/Ca-Calmodulin cause?

A

nNOS activation

75
Q

Which particular receptor is involved in neuronal NT/Ca influx?

A

Glutamate

76
Q

Does an increase in intracellular Ca2+ activate iNOS?

A

no

77
Q

What activates iNOS?

A

Inflammation

78
Q

What happens to NO in the presence of superoxides (O2-)?

A

Peroxynitrite is formed (ONOO-)

79
Q

What can peroxynitrite do to pathogens?

A

Nitrosylate (and kill)

80
Q

What is the overall function of eNOS?

A

Control regional BP, flow and platelet activity

81
Q

What is the overall function of nNOS?

A

Control neurotransmission, LTP, Plasticity, Gastric emptying, Upper airway constriction and erections.

82
Q

What can NO activate?

A

Guanylate Cyclase (GC)

83
Q

What can GC do?

A

Convert GTP to cGMP

84
Q

What effect does cGMP have on vascular muscle?

A

Relax it

85
Q

What effect can Hypercholstermic induced reduction of NO cause?

A

Athergenesis

86
Q

What can a lack of NO result in the formation of?

A

LDL (and thus arthersceloris)

87
Q

What can LDL cause in terms of NO?

A

Decreased L-arginine uptake

88
Q

How do statins reduce risk of atherosclerosis?

A

Decreasing LDL production

89
Q

What (briefly) is angina?

A

Spasm of coronary artery

90
Q

Statins stabilise eNOS mRNA, how does this reduce CVS risk?

A

Increases eNOS expression, decreases platelet activity and vasoconstriction

91
Q

What effect does GTN have?

A

Mimics NO stimulation of Guanylate Cyclase

92
Q

Which receptor does Sildenafil inhibit?

A

Phosphodiesterase V

93
Q

What can sudden and large expressions of iNOS cause?

A

Septic shock

94
Q

What is an inhibitor of iNOS?

A

Glucocorticoids

95
Q

When is ADMA found in higher concentrations?

A

In CVD

96
Q

What does ADMA do?

A

Inhibit eNOS

97
Q

How can ADMA levels be reduced?

A

Exercise

98
Q

What do Kinases do to proteins?

A

Take a Pi from ATP and phosphorylate the protein

99
Q

What are the 3 main types of Kinase-Linked receptors?

A

Receptor Tyrosine Kinase (TRK), Serine/Threonine Kinase and Cytokine receptors (non-TRK)

100
Q

How many transmembrane domains do RTK have?

A

one

101
Q

In RTK, what is the N-terminus?

A

Binding domain

102
Q

In RTK, what is the C-terminus?

A

Kinase domain

103
Q

What are 4 examples of RTK?

A

Insulin receptor, PDGFR, EGFR and TrkA

104
Q

What function are RTK generally associated with?

A

Growth and Development

105
Q

What happens when RTK ligand binds to it?

A

It dimerises with another RTK

106
Q

What does RTK dimerisation cause?

A

Tyrosine residue Autophorphorylation

107
Q

What does tyrosine autophosphorylation cause?

A

It attracts proteins with an SH-2 domain

108
Q

Do cells across the body have the same SH-2 domain protein?

A

No. The same ligand can cause different effects around the body due to differential expression of SH-2 domain proteins.

109
Q

What is PDGFR?

A

Platelet-Derived Growth Factor Receptor

110
Q

What are 3 examples of PDGFR-induced SH-2 proteins?

A

PLC-gamma, GAP and Phosphatase

111
Q

Which cascade do most RTK activate?

A

RAS/MAPK

112
Q

What are the MAPK sequentially acting proteins

A

MAPKKK, MAPKK and MAPK

113
Q

What happens to MAPK in some cancers?

A

It can become defective

114
Q

What happens as a result of defective MAPK signalling?

A

RAS drives oncogenesis as it is permanently bound to the cell membrane

115
Q

The ‘-mab’ suffix indicates what in a drug?

A

Antibody therapy

116
Q

What is the main structural difference between RTK and Cytokine receptors?

A

Cytokine receptors have no Kinase/Enzymatic domain

117
Q

Name 4 main Cytokine receptor types.

A

GM-CSF, Interferon-gamma, Growth Hormone and Interleukin I.

118
Q

What are Cytokine receptors often associated with?

A

Immune and Haematopoietic functions

119
Q

What is JAK/STAT?

A

Janus Kinase/ Signal Transducer & Activator of Transcription

120
Q

When Cytokine receptors dimerise, what does JAK do?

A

It phosphorylates the tyrosine residue

121
Q

What does JAK phosphorylation result in for STAT?

A

They are recruited and dimerised.

122
Q

What happens to dimerised STAT?

A

They translocate to the nucleus

123
Q

What are nuclear receptors?

A

Ligand Gated Transcription Factors

124
Q

In addition to the C and N terminus, what domain do nuclear receptors have?

A

A core DNA binding and recognising domain

125
Q

How are nuclear receptors activated?

A

Intracellular Ligands

126
Q

When nuclear receptors are activated, what happens to them?

A

They dimerise and bind to the Hormone Response Element of DNA (HRE)

127
Q

Name 4 main types of nuclear receptors.

A

Oestrogen receptors, Glucocorticoid receptors, Vitamin D receptor and Free Fatty Acids

128
Q

What are the three main classes of nuclear receptors?

A

Class 1, 2 and Hybrid

129
Q

What are class 1 nuclear receptors?

A

Lipid/Retinoid receptors

130
Q

What are class 2 nuclear receptors?

A

Steroid receptors

131
Q

What are hybrid nuclear receptors

A

Endocrine receptors

132
Q

What are Orphan GPCR

A

GPCR or nuclear receptors of which the ligand has not been identified

Signal Transduction (1 decks)

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