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BI1004 - the dynamic cell > Cell signalling and pharmacology > Flashcards

Cell signalling and pharmacology Flashcards

1
Q

What does cell signalling give the cell the ability to do?

A

Detect or receive info, process info, respond to generate events fundamental to life.

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2
Q

What does cell signalling allow for?

A

Specialist functions, co-ordination with other cells.

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3
Q

Why are signalling molecules and their receptors the main target for therapeutic drugs?

A

Abnormal cell signalling underpins most disease processes.

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4
Q

What do pathogenic organisms and viruses modify?

A

The host’s signalling pathways to use to their own advantage.

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5
Q

What is the breeding behaviour or prairie voles controlled by?

A

The action of related peptides oxytocin and vasopressin - act through specific receptors found in regions of the brain concerned with mating.

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6
Q

What is the first general principle of cell signalling?

A

Cells communicate with each other via extracellular signalling molecules known as first messengers.

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7
Q

How is intercellular signalling undertaken?

A

Signalling cell produces signalling molecule (ligand), can travel short or long, molecule detected by receptor on target cell, receptor specific for molecule, allows control and specialised functions.

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8
Q

What are the two broad classes of extracellular signalling molecules that exist?

A

Large/ hydrophilic (water soluble) - bind to cell surface receptors, small/hydrophobic - enter cell and bind to intracellular receptors.

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9
Q

Why is most cell signalling via cell surface receptors?

A

Majority of signalling molecules are hydrophilic.

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10
Q

What do cells communicate through?

A

Extracellular messenger molecules.

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11
Q

What is the paracrine signalling mechanism?

A

Released signal affects cells in close proximity (local mediators), limited travel ability, e.g. growth factors, histamine.

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12
Q

What is the autocrine signalling mechanism?

A

Sender and target cell are same, e.g. molecules regulating development.

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13
Q

What is the endocrine signalling mechanism?

A

Usually signal acts on distant cells, hormones, e.g. insulin, glucagon, oestrogen etc…

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14
Q

What is the synaptic signalling mechanism?

A

Axon of neurone transmits electrical signal over long distance, at axon terminal signal cause release of neurotransmitter into synapse e.g. GABA, acetylcholine, transmitter travels short distance to target cell.

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15
Q

What is juxtacrine signalling?

A

Signalling cell in direct contact with target - contact dependent.

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16
Q

What is signal transduction linked with?

A

Cell surface receptors?

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17
Q

What is the process of signal transduction?

A

Begins when receptors on cell surface receive signal and convert or relay message to molecule inside cell, signal transduced along may intracellular molecules.

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18
Q

What is signal transduction overall?

A

Process whereby one type of signal is converted into another type.

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19
Q

What is the second general principle of cell signalling?

A

Signal transduction.

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20
Q

What is the third general principle of cell signalling?

A

The response of cell can be fast or slow.

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21
Q

What is the fourth general principle of ell signalling?

A

Same signal molecules can induce different responses in different target cells.

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22
Q

How can the same signal molecules induce different responses in different target cells?

A

Via variants of isoforms of the same receptor, similar receptors use different intracelular signal transduction pathways.

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23
Q

Via what do cells surface receptors relay extracellular signals?

A

Intracellular signalling molecules or pathways.

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24
Q

How does cellular response occur via intracellular pathways?

A

Acts like molecular relay as message transduced from molecule to molecule, final molecule in sequence interacts/activates effector protien.

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25
How is information mainly transferred/relayed in signal transduction pathway?
By changes in state of proteins - change in protein in pathway subsequently detected but next molecule in sequence, in turn becomes altered, so on so forth…
26
What are common alterations in shape changes of proteins induced by?
Molecules simply binding with each other, addition/removal of phosphate to molecule, binds to phosphate on another molecule.
27
What is the point of a signal transduction cascade?
Amplify the original signal, integrate and si tribute signals coming from other pathways.
28
What allow for some signalling components to be activated more efficiently?
Scaffold proteins.
29
What different types of molecules are signal transduction pathways comprised of?
Proteins (enzymes), lipids (phospholipids), small chemical mediators (cAMP), ions (Ca2+), gases (nitric oxide).
30
What do many intracellular proteins that act as signal transduction molecules also act as?
Molecular switches.
31
What do molecular switches do?
Toggle between inactive and active states, comprised of two broad classes.
32
What are molecular switches activated/ deactivated by?
Binding to guanine nucleotides (GTP and GDP), phosphorylation.
33
What regulates the molecular switches known as G proteins?
Binding to guanine nucleotides.
34
When are G proteins active and inactive?
Inactive when bound to GDP, active when bound to GTP.
35
What is the intrinsic GTPase activity of G proteins?
Hydrolysis of GTP to GDP switches off protein.
36
What two forms of G proteins are there?
Within trimeric complex (used by coupled receptors), as a single monomeric protein.
37
Why are monomeric G proteins classed as a superfamily?
~150 members.
38
What does activation and inactivation of monomeric G proteins require?
GEFs to aid in GDP/GTP exchange, GAPs to aid in GTP hydrolysis.
39
What are key members of the monomeric G proteins and their roles?
Ras (cell division and growth), Rab (membrane transport and vesicular transport, Rac/Rho (cytoskeleton organisation migration.
40
How is phosphorylation undertaken by protein kinases?
Add phosphate from ATP to specific amino acids on target protein (tyrosine kinases, serine/threonine kinases).
41
What reverses covalent modification?
Protein phosphatases.
42
What also exists that modified lipids the same as protein kinases?
Lipid kinases and lipid phosphatases.
43
What are protein kinases, how are they organised, what can they do once activated?
Also switch proteins, sequence in signal transduction pathway, can phosphorylate and activate next protein kinase.
44
What produces cAMP?
From ATP by enzyme adenylyl cyclase.
45
What does adenylyl cyclase consist of?
Two transmembrane domains joined by a catalytic intracellular domain.
46
What is cAMP degraded from?
A cyclic nucleotide to a 5’ monophosphate by a cAMP phosphodiesterase.
47
What are most responses to cAMP mediated by?
cAMP-dependent protein kinase.
48
How can cAMP activate PKA?
Inactive PKA has two regulatory subunits and two catalytic kinase subunits, cAMP binds to regulatory ones causing molecule to dissociate, two monomeric kinase units are active and can bind and phosphorylate target proteins.
49
What is PIP2 and where is it found?
Phosphatidylinositol 4,5-bisphosphate, cell membrane phospholipid, found in leaflet of lipid bilayer.
50
PIP2 is a phosphoinositide comprised of what?
Hydrophobic diaclyglycerol (DAG) lipid tail and hydrophilic inositol sugar as head group (inositol triphosphate IP3.).
51
What is used to phosphorylate PIP2 in the lipid bilayer?
PI3-kinase.
52
What is the key regulatory molecule in the phosphorylation of PIP2 via PI3-kinase pathway?
PTEN (phosphatase and tensin homologue on chromosome 10).
53
What does PTEN do and what does this lead to?
Dephosphorylates PIP3 back to PIP2 which shuts down signalling via PKB.
54
What is PDK1?
Phosphoinositol-dependent kinase.
55
What breakdowns PIP2 in the lipid bilayer?
Phospholipase C (PLC).
56
What does activation of a receptor cause in the breakdown of PIP2 in the lipid bilayer?
Activation of phospholipase C (PLC) which cleaves PIP2 into DAG and IP3.
57
What do DAG and IP3 trigger in the breakdown of PIP2?
Activates protein kinase C (PKC), triggers release of Ca2+ respectively.
58
What is the significance of the variation of Ca2+ conc in cytosol?
Constitutes the signal.
59
How are [Ca2+] levels increased?
Influx of Ca2+ from outside cell via channel proteins in membrane, release of Ca2+ from intracellular stores (ER/SR/mitochondria).
60
How are [Ca2+]levels controlled/reduced?
Via ATPase pumps in the plasma membrane and ER/SR/ mitochondrial membrane.
61
What is the structure and function of calmodulin?
Has four Ca2+ binding sites, activated when [Ca2+] increases above 500nm, Ca2+bound calmodulin binds and activity of its target proteins.
62
What are the several number of ways that termination of signalling events can occur by?
Eliminate extracellular signalling molecule (enzyme degradation), deactivate signal transduction molecules (de phosphorylation by phosphatases, degradation by enzymes), remove activated receptor from cell membrane by endocytosis.
63
How are receptor and signal molecules (ligands) internalised?
Either receptor and signalling molecule are separated and receptor is recycled to surface and ligand destroyed or the receptor and ligand are both destroyed.
64
How does a signalling molecule exert its effects?
Binds to specific receptor to ensure specificity of response, cell can also influence response by regulating number of receptors, synthesising different isoforms of receptor.
65
What is an agonist?
A molecule that binds and activates receptor, inducing signalling and a biological response, full agonist = full activation, partial = partial etc…
66
What is an antagonist?
A molecule that binds to a receptor but does not induce signalling and a biological response.
67
What are the three types of cell surface receptors?
Ion channel linked receptors, G protein coupled receptors, enzyme-linked receptors (intrinsic enzyme activity + recruit enzyme from cytoplasm).
68
What are ion channel-linked receptors and what do they do?
Act as gates, ligand binding causes receptor to change shape and open gate, ion flow passively through.
69
How can ion channel-linked receptors by pharmacologically modified?
Channel blockers (physically block), channel modulators (enhance or inhibit).
70
When does synpatic transmission end?
When the neurotransmitter is either taken up by the synaptic terminal or degraded.
71
What are GPCRs?
Largest family of cell surface receptors in biology, bind an enormous range of extracellular signalling molecules.
72
How many GPCRs are there in humans?
~800 - at least twice as many in other mammals.
73
What do GPCRs do?
Mediate a wide array of physiological processes (including odorant detection).
74
What is the similar structure of all GPCRs?
Extracellular ligand binding region, seven alpha helices that span the membrane, intracellular portion interacts with a trimeric G protein.
75
What do GPCRs use trimeric G proteins to do?
Relay the signal.
76
What are the three subunits of trimeric G proteins and which one is used to bind GDP/GTP for GTPase activity?
Alpha (a), beta (B), gamma (y) - Ga (alpha).
77
What are the first three steps of the signal relay via the GPCR?
Binding of ligand alters the conformation of the receptor, Ga unit binds to receptor, binding allows release of GDP and its exchange for GTP.
78
What are the final two steps of the signal relay via the GPCR?
Alpha subunit is active and dissociates from beta and gamma units, both active Ga subunit and By complex can now interact with effector molecules to relay signal - focus on Ga subunit.
79
How are signals relayed using G proteins?
GTP bound activated Ga unit binds to effector molecules altering its activity.
80
What are the steps to switching off G proteins?
Ga subunit hydrolyses GTP to GDP - occurs in seconds - can use RGS protein to aid hydrolysis, Ga dissociates from effector molecule, a subunit having returned to its original GDP inactive conformation can reassemble with By complex to form inactive trimeric G protein.
81
What does RGS stand for?
Regulator of G proteins signalling.
82
What determines which of the numerous classes a Ga exists in?
By which effector molecule the Ga subunit couples with and resulting effect.
83
How many known classes of Ga units coupling to various effector molecules are there?
23.
84
What are the three most common classes of G proteins?
GaS, Gai, Gaq?
85
What is the effector molecule and effect of GaS units?
Adenylyl cyclase, stimulation increases cAMP.
86
What is the effector molecule and effect of Gai units?
Adenylyl cyclase, inhibition decreases cAMP.
87
What is the effector molecule and effect of Gaq units?
Phospholipase C, stimulation increases DAG and IP3.
88
How does the GPCR signalling pathway ‘adrenaline mediated breakdown of glycogen’ work?
Rapid response, signalling pathway amplifies original signal, PKA can also enter nucleus and effect transcription factors involved in mediating longer term coordinated events in biological response.
89
How can G protein signalling be dysregulated?
Cholera toxin binds to GaS and fixes it in GTP bound conformation, over stimulation of adenylyl cyclase and cAMP production, downstream signalling effects transporters involved in ion transport leading to water loss.
90
How can cholera be treated?
Neutralisation of cholera toxin with nano particle decoys for treatment.
91
What activates phospholipase C and what does this do?
GPCRs that are coupled to the Gaq class of G protein, induces Ca2+ mediated events.
92
What are the most well studied receptors with intrinsic enzyme activity?
The receptor tyrosine kinases (RTKs).
93
What do RTKs consist of?
Extracellular domain which binds the ligand, transmembrane domain, intracellular or cytoplasmic domain which contains the tyrosine kinase site.
94
What do tyrosine kinases do?
Add phosphate groups from ATP to only tyrosine residues on target proteins.
95
What are the two classes of protein kinases that exist in animal cells?
Tyrosine kinases and serine/threonine kinases.
96
How are RTKs activated?
Requires dimerisation of two receptor monomers, activates tyrosine kinases in each receptor, kinase phosphorylates tyrosines on opposite receptor tails, recruitment/binding of adaptor and/or effector signalling molecules directly to the phosphorylated tyrosines to initiate signalling.
97
What are some examples of key adaptors/ effectors in the activation of a RTK?
Adaptors - Grb2, Shc, IRS-1, effectors - PI3-kinase, phospholipase C.
98
What do RTK’s commonly utilise to relay or transduce the signal?
The monomeric G proteins signalling Ras.
99
How do RTKs utilise the monomeric G protein Ras to relay or transduce the signal?
Activated receptor either directly or indirectly (via an adaptor protein) binds and activates the GEF for Ras, thereby activating this key signalling molecule.
100
What are the steps of regulation of glucose uptake in muscle and fat cells via activation of the insulin receptor?
Glucose transporters stored in walls of cytoplasmic vesicles, insulin induced IRS-1/PI-3 kinase/PKB signalling triggers vesicle translocation to the plasma membrane, vesicle fuse with membrane where they take up glucose and pass it into cell.
101
What effects does insulin induced signalling have?
Multiple cellular effects which also include decreasing glycogen metabolism and promoting glycolysis.
102
What do cytokine receptors recruit to help initiate signal transduction?
Janus kinase (JAK).
103
What are the mechanisms of action of cytokine receptors recruiting Janus kinase to initiate signal transduction?
Cytokine receptors lack intrinsic kinase activity, recruit soluble tyrosine kinases, ligand binding.
104
What does ligand binding (e.g. prolactin) cause during cytokine receptors using JAK?
Receptor dimerisation and JAK recruitment/activation, JAKs phosphorylate each other/receptor, recruitment of STAT transcription factor to phosphorylate tyrosine residues on receptor.

BI1004 - the dynamic cell (11 decks)

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