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Y2 Mol Bio > Communication and Signalling > Flashcards

Communication and Signalling Flashcards

1
Q

What are the 3 basis of communication?

A

speed
mechanism
duration

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2
Q

Give two examples of contact-dependent signalling

A

Dropophila eye discs are regularly spaced as they differentiate and inhibit each other

Nerve cells

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3
Q

Give two examples of paracrine signalling

A

Mast cells releasing cytokines
Hedgehog (gene) expression stimulates Dpp

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4
Q

Give to examples of endocrine signalling

A

Pheromones can send signals to control hives
Adrenaline produces the “fight or flight” response

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5
Q

Give three actions of effectors

A

Alter metabolism
Alter gene expression
Alter cell shape or movement

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6
Q

Describe the morphogen gradient

A

Responses to signals are different depending on the concentration of morphogen. Cells commit to certain differentiations at different morphogen thresholds

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7
Q

What causes myeloproliferative neoplasms (bone marrow producing too many blood cells)

A

The JAK2 V617F mutation in the negative regulatory pseudokinase domain on JAK2

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8
Q

What causes chromic myeloid leukaemia?

A

BCR-Abi fusion protein causes sustained tyrosine kinase expression by Bcr enhancer/promotor

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9
Q

Compare the speeds of ion channel movement, changing protein levels via gene expression and phosphorylation

A

ion channels- fast
phosphorylation- quite fast
changing protein levels via gene expression- relatively slow

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10
Q

What are the major groups of eukaryotic kinases?

A

S/T kinases
Y (threonine) kinases

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11
Q

What is the receptor tyrosine kinase for epidermal growth factor (EGF)

A

Epidermal growth factor receptor (EGFR)

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12
Q

Describe the type I and II inhibitors of S/T kinases

A

Type I- binds the active conformation at an aspartate pointing to the ATP-binding pocket
Type II- binds inactive conformation

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13
Q

Describe type III and IV inhibitors of S/T kinases

A

Type III- binds to an allosteric pocket adjacent to the ATP binding pocket
Type IV- bind to an allosteric pocket away from the active site

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14
Q

What are the 4 main functions of receptors?

A

Recognise stimuli and transfer it into the cell
Amplify the cytoplasmic signal
Modulate effector systems
Adapt the system through feedback

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15
Q

How can the molecular nature of the signal transduction mechanism be predicted?

A

Not just the stimulus
Class/structure of the receptor

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16
Q

What sort of chemical mediators can hormones bind to?

A

Hormones
Neurotransmitters
Antibodies

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17
Q

Describe a general structure of ion channels

A

Transmembrane protein made of 2 or more α-helices crossing the lipid bilayer
2-6 subunits surrounding a pore

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18
Q

How are ion channel subgroups characterised?

A

Gating mechanism
Ion selectivity

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19
Q

What is a p-loop/pore?

A

Pocket where ion binds

20
Q

Describe the structure of KcsA as a model for primordal channels

A

TMs are more more tightly packed on the cytoplasmic side, creating a gate
3 subunits: 2TM helices, 1 extracellular domain

21
Q

Describe KvaP structure

A

S1-S4 TMs form a voltage sensing domain. S5 and S6 form the pore
Plugging mechanism stops ions entering

22
Q

What are transient receptor potential (TRP) channels

A

Sense chemical and physical stimuli. e.g hot/spicy food
Common structural features with voltage-gated channels

23
Q

Where does calmodulin bind on an ion channel?

A

The C-terminal cyclic nucleotide-binding domain

24
Q

Describe the structure of ligand-gated ion channels

A

Gated
4 subunits
6 TM helices
P-loop
Cytoplasmic anchors

25
Q

Describe the structure of transient receptor potential channels

A

Gated
4 subunits
6 TM helices
P-loop
Cytoplasmic anchors
Plugging mechanism

26
Q

Describe the structure of voltage-gated ion channels

A

Gated
4 subunits
6-24 TM helices
P-loop
Cytoplasmic anchors
Voltage-sensing domains
Plugging

27
Q

Describe the structure of simple channels

A

Not Gated
2 subunits
2 TM helices
P-loop

28
Q

Describe ATP P2X structure

A

Trimeric
2 TM
ATP binding site in the extracellular domain

29
Q

Describe glutamate receptor structure

A

Tetrameric - form as a dimer of dimers
Extracellular domain
3 TM and a half-helix
Similar structure to KcsA, except an inverted pore

30
Q

Describe nicotinic receptor structure

A

Pentameric
4 TM
Extracellular domain recognising neurotransmitters

31
Q

What neuronal nAChRs are important in nicotine addiction?

A

α4β2 are abundant in the cortex and hippocampus. These have a high affinity to nicotine and varenicline

32
Q

What mutations are associated with tobacco dependence?

A

Polymorphisms in subunit genes CHRNA4 (α4) and CHRNA6 (α6)

33
Q

What causes autosomal dominant nocturnal frontal lope epilepsy (ADNFLE)?

A

Mutations in the M2 domain (channel gate) of the human α4 neuronal subunit of the nicotinic acetylcholine receptor. This increases nicotinic-mediated transmission

34
Q

What are the symptoms of ADNFLE?

A

Epilepsy which occurs during sleep. Delayed response in receptors. increased nicotinic-mediated transmission

35
Q

What do AMPA receptors mediate?

A

Fast excitatory synaptic transmission in the CNS

36
Q

What do NDMA receptors mediate?

A

Learning and memory. These are slower than other isoforms

37
Q

What are kainate receptors linked to?

A

Schizophrenia, depression and huntington’s
Similar to AMPA

38
Q

How does RNA splicing affect splicing isoforms?

A

Each subunit is encoded by a splicing isoform- flip/flop
Alternative splicing takes place in the primary transcripts
The isoforms have different kinetic properties- flop has faster desensitisation rate and reduced current responses to glutamate than flip

39
Q

Why is RNA editing important in M2 (parasympathetic, in the heart) receptors?

A

Inside the channel pore is the GluA2 Q/R site. RNA editing converts Glu to Arg, blocking Ca2+ channel permeability

40
Q

What happened to mice lacking RNA editing?

A

Prone to seizures and early death due to Ca2+ channel permeabilities not changing

41
Q

What are NDMA receptors associated with?

A

Synaptic plasticity, learning and memory

42
Q

How does ALS cause neurodegeneration?

A

The enzyme ADAR2 is downregulated, preventing GluA2 Q/R editing in motor neurons. Ca2+ permeability increases in AMPA receptors, damaging glutamate excitotoxicity

43
Q

How does ALS cause neurodegeneration?

A

The enzyme ADAR2 is downregulated, preventing GluA2 Q/R editing in motor neurons. Ca2+ permeability increases in AMPA receptors, damaging glutamate excitotoxicity

44
Q

What is decreased ADAR2 activity correlated with?

A

Cancer cells in glioblastoma
Ca2+ permeability increase in AMPA receptors

45
Q

Describe P2X receptors

A

3 ATP gated to open the ion channel
3 subunits- 2 TM helices

46
Q

Give three examples of P2X receptors targeted by drugs

A

P2X2- hearing loss
P2X4- pain
P2X7- inflammation

Y2 Mol Bio (10 decks)

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