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BIOL1013 > Cell signalling and receptors > Flashcards

Cell signalling and receptors Flashcards

1
Q

What are the types of signals that can be produced?

A
  1. Mechanical
  2. Biochemical
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2
Q

For a biochemical signal, what is required?

A

A ligand and a receptor

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3
Q

What is a signal ligand?

A

a small molecule that forms a complex with a macromolecule typically a receptor protein that results in a conformational change in the receptor that then generates a signal

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4
Q

Tell me 3 different forms of signal

A
  1. Contact- dependent signals
  2. Cell-matrix signals
  3. soluble signals; Autocrine, Paracrine, Endocrine
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5
Q

Tell me about Contact- dependent signals (juxtacrine)

A
  • require interaction between membrane molecules on two cells
  • cells must be touching
  • signals are transmitted through cell membranes via protein or lipid componenets integral to the membrane of the emitting cells
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6
Q

Tell me about Cell-matrix signals

Provide some examples of them

A
  • insoluble signalling molecules

examples;

a. Mesenchymal cells (neurons, muscle cells, fibroblast) are surrounded by a matrix

b. Chondrocyte cell surrounded by matrix (cartilage)

c. Cell-matrix interactions can be organised at focal contacts

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7
Q

Where is an epithelial cells matrix found?

A

Only on one side

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8
Q

Tell me about Autocrine signals

Provide some examples

A

They are secreted and affect the target cell itself via its own receptors

Examples;

1. Interleukin-1; a cytokine released by macrophages. effects neighbouring cells and the secreting cell “activating them”

2. Interleukin-2; is released by T lymphocytes on meeting an antigen and causes them to proliferate

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9
Q

Tell me about intracrine signals

provide an example

A

They are produced by and stay within target cells (a version of autocrine signalling)

Examples

  1. adipose tissue
  2. some steroid hormones have their receptors in the cell so can act as intracrine (and paracrine and endocrine signals)
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10
Q

Tell me about Paracrine signals

Provide some examples

A

These signals target cells in the vicinity of the emitting cell

They are localised signals

Examples

  1. Immune cells; neurotransmitters at synapses
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11
Q

Tell me some local mediators of paracrine signals which are released into the interstitual fluid

A
  1. Histamine
  2. TGFß
  3. Growth factors
  4. cytokines
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12
Q

Are chemical synapses- neuronal signals paracrine signals?

A

yes

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13
Q

Tell me about Endocrine signals

Provide an examples

A

They target distant cells by producing hormones that travel through the circulation to reach all parts of the body

Examples

  1. adrenalin
  2. thyroid stimulating hormone
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14
Q

Tell me some hormones and their concentration at low concentration in the blood/interstitual fluid

A

Thyroxine 0.09-20 pg/ml

Oestrodiol 20-400 pg/ml

Prolactin 3-15 ng/ml

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15
Q

What is 1pg in grams…

1 Pg = … g

A

1 pg= 1x10-12 g

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16
Q

Tell me about the affinity of hormone receptor binding

A

Has a far greater affinity (low Kd) compared to others

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17
Q

What are hormone receptors part of?

A

amplification cascades

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18
Q

Tell me some chemical classification of external messengers and examples for each

A

Gases: NO, CO, H2S, CO2.

Nucleic Acids: ATP, ADP and adenosine.

Fatty acid derivatives: Eicosanoid e.g. prostaglandins, thromboxanes, leukotrienes, PAFs.

Cholesterol derivatives: steroids

Amino acids and derivatives: glycine, glutamate, thyroid hormones, catecholamines- e.g. adrenaline

Peptides: e.g. TRH

Proteins: e.g. Insulin

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19
Q

What are gases produced by ?

A

specific enzymatic pathways

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20
Q

Tell me about the solubility of gases and what this allows them to do/ not to do

A

They are highly soluble in water and lipids

Can cross plasma membrane

can’t be stored

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21
Q

Are gases only made when they are needed ?

A

yes

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22
Q

What type of local effects do gases produce?

A

Paracrine and autocrine effects

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23
Q

What type of responses do they produce?

A

Generally, cause vasodilation and may have immunological effects

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24
Q

Tell me what nucleic acids function as paracrine signalling molecules

A

The purinergic nucleotides ATP/ADP and their nucleoside adenosine

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25
Q

What do nucleic acids specifically have and what is this associated with?

A

Have specific cell surface receptors

Have G proten associated with them

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26
Q

What happens with nucleic acids during cellular stress (e.g. ischemia /reperfusion or inflammation) ?

A

multiple cell types release ATP into the extracellular space

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27
Q

What type of effects do nucleic acids have?

A

Vasodilation, neural effects (in development), innate immune changes e.g. inflammatory cytokine release, fever

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28
Q

As the fatty acid derivatives are polar, what does this mean for their transport?

A

They don’t rapidly cross the cell membrane so have receptors

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29
Q

Tell me some examples of polar fatty acid derivatives

A

PAFs and Eicosanoids e.g. prostaglandins, thromboxanes, leukotrienes

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30
Q

What type of signals do fatty acid derivatives produce?

How are they produced?

A

Paracrine signals

Produced through modification and release of lipids in the plasma membrane

Eicosanoids – arachidonic acid

Platelet activating factor-phosphorylcholines

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31
Q

Tell me some roles of fatty acid derivatives

A

Regulate immune responses, inflammation (vascular permeability), pain reactions, vasoconstriction/ dilation and clotting

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32
Q

Cholesterol derivatives are hormones that are transported by the circulatory system to target distant organs.

Give some examples of these hormones

A

Sex (gonadal/ placental) steroids: Oestrogens, Progesterone’s, Testosterone.

Adrenal steroids: Mineralocorticoids (aldosterone) Glucocorticoids (cortisol)

Vitamin D: (can’t make this, but its structure is that of a steroid so classed as this)

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33
Q

Are cholesterol derivatives produced on demand ?

A

yes

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34
Q

Cholesterol aren’t very water soluble so how are they transported?

A

May have a carrier in the plasma

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35
Q

Where are cholesterol derivatives receptors found and why?

A

Main receptors are inside the cell and not at the membrane as they are lipid soluble molecules so readily cross the membrane

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36
Q

What are amino acid derivative produced by ?

A

exocytosis

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37
Q

Are amino acid derivative relativelt lipid soluble?

A

no, they are lipid insoluble

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38
Q

Tell me some amino acid, paracine, neurotransmitters and whether they are excitatory or inhibitory

A

Glutamate, Aspartate: excitatory

Glycine: inhibitory

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39
Q

Amino acid derivative are active Biogenic amines, how are they produced?

A

by the decarboxylation of amino acids

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40
Q

Give 3 examples of amino acid derivatives?

A
  1. Histamine
  2. GABA
  3. Serotonin
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41
Q

Tell me what amino acid Histamine is derived from and its Histamines role?

A

Derived from Histidine (paracrine)

role: immune responses, vasodilation, acid secretion in GI tract, neurotransmitter

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42
Q

Tell me what GABA (gamma-aminobutyric acid) is derived from and GABA’s role ?

A

Derived from; glutamate (paracrine)

role; inhibitory neurotransmitter

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43
Q

Tell me what serotonin is derived from, and serotonins role?

A

dervided from; tryptophan

role; neurotransmitter, vasodilation

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44
Q

When are Catecholamines produced and give 3 examples and their roles?

A

produced after tyrosine decarboxylation

Examples and their roles;

  1. Dopamine; Neurotransmitter
  2. Noradrenaline; Neurotransmitter
  3. Adrenaline; Hormones and neurotransmitter
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45
Q

Tell me another tyrosine modification

A

conjugated/ iodinated hormones

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46
Q

When decarboxylating an amino acid, what is the enzyme?

A

Histidine Decarboxylate

(The name of what enzyme was decarboxylated)

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47
Q

What is the largest class of signalling molecules?

A

Peptides and proteins

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48
Q

What is the range in sizes of peptides and proteins?

A

from 3 AA (e.g. TRH= Glu-His-Pro-(N) to growth hormone e.g. GH~ 200 AA

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49
Q

Peptides and proteins are not soluble in lipids, what term is used to describe this?

A

Lipophobic

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50
Q

Tell me 3 types of signal molecules?

A
  1. Lipophilic (hydrophobic) molecules
  2. Hydrophilic molecules
  3. Tyroid hormones
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51
Q

Tell me about Lipophilic (hydrophobic) molecules and give some examples

A

like to be in lipid not aq environment

e.g. Steroids (cortisol) and Gases (NO).

Can enter the cells so the receptors can be anywhere, often within the cytosol. (sometimes found in nucleus)

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52
Q

Tell me about hydrophilic molecules and give some examples

A

e.g. Amines (serotonin), Amino Acids (Glycine), Peptides (ACTH) and Proteins (Insulin).

Can’t cross the plasma membrane so receptors at the cell surface.

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53
Q

Tell me about thyroid hormone

A
  • are Hydrophobic
  • have a carrier at the cell surface to bring the ligand into the cell
  • have receptors in the cytoplasm
  • An amino acid derivative (produced from tyrosine)
  • An exception
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54
Q

Compare intracellular signal receptors and cell membrane receptors

A
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55
Q

Define signal transduction?

A

How chemical or physical signals are transmitter through a cell as a series of molecular events

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56
Q

How are chnages elicited in signal transduction and what does this cause?

A

The changes elicited by ligand binding to a receptor which gives rise to a signalling cascase, a chnage of biochemical events- a signalling pathway

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57
Q

signalling pathways may interact with one another to form networks, which allow coordinated cellular responses. Give some responses?

A
  • changes in the transcription or translation of genes.
  • Don’t act in isolation
  • post-translational and conformational changes in proteins.
  • changes in protein location.
  • changes in ion concentration.
  • alter cell growth
  • proliferation
  • metabolism
  • movement
  • secretion
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58
Q

What are First messengers?

A

signalling molecules (hormones/ paracrine/ autocrine agents) that reach the cell from the extracellular fluid and bind to their specific receptors.

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59
Q

What are second messengers?

A

substances that relays message from the plasma membrane to the cytoplasm to trigger a response.

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60
Q

What do cell surface receptors need?

A

second messengers

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61
Q

Examples of second messengers…

A
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62
Q

Give 3 examples of lipophilic signalling?

A
  • NO (nitric oxide)
  • Steroids
  • Tyroxine
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63
Q

Give examples of plasma membrane receptors for hydrophilic signalling?

A
  • Ligand-gated ion channels (e.g. nicotinic acetylcholine receptor)
  • G-protein-linked receptors (β-adrenergic receptor)
  • Enzyme-linked receptors (growth factor receptors)
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64
Q

What type of signal molecules is NO ?

A

A Non-polar local mediator

65
Q

Why cant NO be retained in vesicle stores?

A

Its lipophilic

66
Q

What happens to NO directly after synthesis?

A

It immediately leaves its site of synthesis and diffuses into all adjacent cells

67
Q

What cells does NO only affect?

A

Those with an NO receptor

68
Q

Why is NO known as a local mediator

A

its broken down quickly so doesnt get very far after synthesis

69
Q

What is NO produced from?

A

Arginine

70
Q

What does the production of NO depend on?

A

NO synthase

71
Q

What are the 3 forms of NO synthase (NOS) and where is each found/ used?

A
  1. eNOS - blood vessel endothelial cells
  2. nNOS - neuronal cells
  3. iNOS - inducible isoform occurring in cells of the immune system
72
Q

NO produced by eNOS helps control what?

A

control the diameter of blood vessel’s hence and blood pressure

73
Q

For eNOS, what is the endothelia stimulated by?

A
  • Histamine
  • Acetylcholine (from nerve endings)
  • Increased sheer flow
74
Q

When NO diffuses into the smooth muscle, what effects does it cause?

A
  • Vasodilation
  • Reduced blood pressure
75
Q

In NO signalling, whats the target for NO?

A

Guanylate cyclase

NO binds to active site of guanylate cyclase and activates it

76
Q

In NO signalling, cGMP is produced, what does this act as and what does it cause?

A

This acts as a second messenger and causes relaxation

77
Q

Tell me the steps to how cyclic cGMP causes muscle relaxation?

A
  • Blocks Ca2+ entry into the cell by phosphorylating Ca2+ channels, decreasing intracellular calcium concentrations inhibiting myosin-actin interactions.
  • Phosphorylates and activates K+ channels, which leads to hyperpolarization and relaxation.
  • Phosphorylates and activates myosin light chain phosphatase (phosphatase removes the phosphate), this phosphorylates myosin chains and causes smooth muscle relaxation.
78
Q

When NO is rapidly oxidised to NO3-, what does this mean?

A
  • rapid spontaneous breakdown (a short-lived signal)
  • Guanylate cyclase is inactivated
79
Q

what is cGMP converted to GMP by?

What happens in the bonds for this reaction to happen?

A

cGMP is converted to GMP by the enzyme phosphodiesterase (11 isoforms) - breaks the phosphodiesterase bond with the 3’OH ribose

80
Q

How does Viagra work?

A

Sildenafil (Viagra) blocks the action of phosphodiesterase 5, prolonging the relaxation of blood vessel smooth muscle in the penis - treatment of impotence

81
Q

What is the role of phosphatases?

A

Phosphorylated downstream enzymes converted back to original form by phosphatases

82
Q

What type of hormones are steroids?

A

hydrophobic

83
Q

What are steroids synthesised from?

A

synthesised from cholesterol and are immediately released

84
Q

Why can’t steroids be stored?

A

They are hydrophobic

85
Q

Where are steroids released into and where do they travel to ?

A

They are released into the blood and are carried into tissues. they then readily diffuse into cells where they bind to cytoplasmic receptors

86
Q

When steroids bind to their receptors, what sites does it unmask?

A
  • DNA binding sites
  • nuclear localisation sites
87
Q

How is the steroid signal removed?

A

metabolism of the steroid

88
Q

Steroid release process

A
89
Q

As seen below, steroids have very similar structures, why are the effects so different?

A

Even though structure Is similar, the effects are very different because the receptors are very specific.

90
Q

What is the testosterone receptor also known as?

A

The androgen receptor NR3C4

91
Q

What does the mutation of the testosterone receptor lead to?

A

it prevents or reduces testosterone signalling despite the presence of the hormone

Male individuals (XY) with mutated androgen (testosterone) receptors are incapable of signal transduction thus are biologically male, but phenotypically immature male or female

92
Q

Tell me about thyroxine signalling?

A
  • The thyroid hormones can’t cross the cell membrane but have transporters to bring them into the cell.
  • They then diffuse into the nucleus
  • Once in the nucleus they act in a similar manner as steroids – however their receptors are already in the nucleus
93
Q

What drives the movement of Ions across the plasma membrane?

A
  • concentration gradient
  • electrochemical gradient
94
Q

When the ligand gated ion channel is opened what does this cause?

A

A change in ion concentration at the inner side of the membrane fast and change potential difference (Na+/ K+) - this is very localised and quick

95
Q

when some ions bind to proteins, what can it cause?

A
  • conformational changes
  • signal transduction
96
Q

Tell me some facts about signalling?

A
  • Rapid- milliseconds
  • Localised- only region close to opening of the channel (unless amplified)
  • can be quickly reveted to normal
97
Q

Give some examples of some FAST ligand-gated ion channels

Out of those listed, which bind and activate different types of receptors?

A

Nicotinic acetylcholine receptor

Glutamate receptor

Seratonin (5HT) receptor

GABA receptor

Glycine receptor

Extracellular ATP receptor

(bind and activate different types of receptors)

Important: Most of these ligands can bind to other types of receptor - G-protein linked receptors exist for all these ligands except glycine and ATP.

98
Q

What can the Nicotinic Acetylcholine receptor bind?

A

Nicotine and Ach

99
Q

What does the nicotinic acetylcholine receptor belong to and what is this?

A

Belongs to the superfamily of ligand-gated ion channels (thought to have evolved from a common ancestor)

100
Q

The nicotinic acetylcholine receptor is a pentamer made of what differing subunits?

A

α2βγδ or α2β3

101
Q

What binds to the muscarinic receptor?

A

only Ach

102
Q

Tell me about the structure of the nicotinic acetylcholine receptor?

A
  • 5 polypeptides α2βγδ or α2β3.
  • Each polypeptide contains 4 alpha helices.
  • 3 are mainly hydrophobic and contact the lipid membrane.
  • 1 of these (M2) is an amphipathic helix and lines the pore (regions of hydrophobic and hydrophilic). If M2 are lined up together you can form a channel which allows cold water to pass through but not hot
  • The 5 amphipathic helices produce a channel across the membrane
  • The α subunits have the acetylcholine binding regions.
  • Conformation changes on binding of 2 acetylcholine molecules.
103
Q

When Ach binds to the Nicotinic acetylcholine receptor, what happens?

A

the helices rotate which pulls the charged residues from the pore which opens it

104
Q

When ligands bind to the Nicotinic acetylcholine receptor what happens?

A

causes transient (fast) opening of the channel to allow the cations to enter (Na+, Ca2+, K+)

It is non-selective but is particularly permeable for Na+ and K+. However, it is mainly Na+ ions that pass.

105
Q

Why can’t anions enter the nicotinic acetylcholine receptor?

A

The size and polarity of the pore blocks larger and negatively charged ions

106
Q

Tell me the about the concentrations of K+, Na+ and Cl- intracelluarly and extracelluarly?

A
  • The membrane potential of excitable cells is around –70mV (negative in).
  • The effect of opening the Nicotinic receptor is predominantly an inflow of Na ions due to the electrochemical gradient.
107
Q

when Ach receptor opens, why does the membrane become depolarised?

A

As Na+ ions enter the cell

108
Q

Tell me about generation of an action potential?

A
  • When the acetylcholine receptors are opened the membrane becomes depolarised as Na+ ions enterthe cell.
  • If sufficient are opened, adjacent voltage-gated sodium channels sense the depolarisation of the membrane.
  • These transiently open causing a wave of depolarisation (this is the action potential) to sweep across the cell membrane triggering events in distant parts of the cell
109
Q

Tell me what happens when the following channels are opened?

  1. Na+
  2. K+
  3. Cl-
A
  1. Opening Na+ channels will depolarise the cell as the membrane potential and sodium gradient result in Na+ entering the cell.
  2. Opening K+ channels will hyperpolarise the cell as K+ leaves the cell.
  3. Opening Cl- channels will hyperpolarise the cell as Cl- enter
110
Q

Name some other ligand gated ion channels

A
  • Serotonin (5-HT3) receptors (cation channel)
  • Ionotropic glutamate receptor (cation channel)
  • GABAA receptor (chloride channel)
  • Glycine (chloride channel)

When chloride channels open the membrane hyperpolarises, this counteracts the excitability of the membrane caused by the binding of ligands that open cation channels

111
Q

Name the 3 major classes of receptors and give examples for each

A
  1. Ligand-gated ion channels (e.g., nicotinic acetylcholine receptor)
  2. G-protein-linked receptors (β-adrenergic receptor)
  3. Enzyme-linked receptors (growth factor receptors)
112
Q

What kind of structure do G-protein linked receptors have?

A

They all have a 7 pass structure (cross the membrane 7 times)

Big loop between 5 and 6

113
Q

Tell me some roles of G-protein linked receptors

A
114
Q

What type of complex is the G-protein complex?

Why is it called this?

A

It is a Trimeric complex

contains;

  • alpha
  • beta
  • gamma
115
Q

Where are all the parts of the G complex attached to?

A

The inner side of the plasma membrane

116
Q

What does the alpha unit of a G complex contain?

A

A GTP/GDP binding site

and

GTPase activity

117
Q

When is the alpha subunit active/ inactive?

A

When GTP is bound, an active signalling complex is formed

When converted to GDP (or no nucleotide is bound) it is inactive

118
Q

Whats the equation for the formation of GDP and what the enzyme involved in this?

How long does the reaction take?

A
119
Q

What does GDP help to reform?

A

The trimeric complex

120
Q

Are there large and small G proteins?

A

yes

121
Q

What are the large G proteins also known as?

A

αβγ

122
Q

Tell me the function/ importance of the large and small G proteins ?

A

Large proteins: Link to the inner plasma membrane and associate with receptors

Small proteins: importatn for downstream events in signal transduction and wont be discussed in course

123
Q

Can active signalling complexes be active for a large range of time?

A

yes

124
Q

In the inactive atate what is GPCR bound to?

A

A Heterotrimeric G protein complex

125
Q

When a ligand binds to the extracellular surface of the GPCR what does this cause?

A

It results in a conformational change in the receptor that is transmitted to the bound Galpha subunit

it causes the Galpha subunit to release GDP and exchange it for GTP

126
Q

When GDP is released what does this trigger?

A

The dissociation of Galpha subunit from the GßY dimer and from the receptor- both are active complexes

results in two active signalling complexes

127
Q

What do G proteins dissociate into when activated?

A

2 signalling proteins

Galpha and GßY

128
Q

How many different forms are there of;

  • Galpha
  • Gß
  • Gy
A

20 different forms of Galpha

5 different forms of Gß

13 different forms of Gy

129
Q

What do the different forms of G protein subunits show their differences in?

A
  • expression patterns
  • receptor binding
  • effects produced in the cell
130
Q

What does the differences between the G protein subunits mean?

A
  • specificity to their signals
131
Q

What are the different type of Galpha subunits are there?

What do each activate/ inactivate?

A
  1. Gas: activates adenylyl cyclase
  2. Gai: Inactivates adenylyl cyclase
  3. Gaq: Activates Phospholipase C
132
Q

When the Gas activates adenylyl cyclase, what receptor does it bind to?

A

ß- adrenergic receptor

133
Q

What is the role of Adenylate cyclase?

A

It converts ATP to the second messenger cyclic AMP (cAMP)

134
Q

Whats the role of cAMP?

A

Activates a protein kinase called protein kinase A (PKA)

By binding to the regulatory subunits of the proteins which causes the release of the active catalytic subunits

135
Q

Whats the amplification step is Gas process?

A

ATP –> cAMP

136
Q

Write the reaction for ATP–> cAMP and the enzymes/ products involved

A
137
Q

Can cAMP signalling have fast and slow effects?

A

yes

138
Q

Write the equation which demonstrates the rise of cAMP concentration following the application of the signalling molecules of serotonin

A
139
Q

Name a ligands that activates adenylyl cyclase

A

adrenaline

140
Q

In some prostglandin receptor, what can Gai inactivate?

A

the membrane bound enzyme adenylyl cyclase

141
Q

What does the subunit Gai reduce?

A

The second messenger cAMP

142
Q

Whats happens when a hormone such as ADH binds to Gaq?

A

E.g. Antidiuretic Hormone can bind to a G-protein-linked receptor.

In this case the activated Gα-subunit switches on the enzyme phospholipase C which cleaves the lipid phosphatidylinositol 4,5-bisphosphate (PIP2) (a phospholipid component of the bilayer).

Forms 2 second messenger’s inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG)

143
Q

How does Ach activate 2 signalling pathways?

A

by activating phospholipase C

144
Q

What does inositol 1,4,5-triphosphate (IP3) act as?

How does it do this?

A

A second messenger

How:

  • IP3 releases Ca2+ from stores in the endoplasmic reticulum.
  • cytoplasmic [Ca2+] rises from 0.1 to 10 μM (x100)
  • Ca2+ + DAG activate protein kinase C.
  • Protein kinase C activates a number of protein targets, including proteins involved in transcription (turning on the expression of particular proteins)
  • Inactivated by converting to metabolites in the cell
145
Q

How does Calcium activate Calmodulin dependent kinase (CaM-kinase)?

A

It binds to the protein calmodulin

146
Q

whats the role of CaM kinase?

A

Regulating the activity of many proteins including some involved in transcription

147
Q

What are the 2 main classes of enzyme-linked receptors?

A
  1. Receptor tyrosine kinases
  2. Receptor serine/ threonine kinases
148
Q

Whats the largest class of enzyme-linked receptor?

Give an example?

A

Largest class are the receptor tyrosine kinases (about 60 different receptors)

e.g. insulin or fibroblast growth factor (FGF) receptor, HER2

149
Q

Give some examples for the receptor serine/ threonine kinase

Whats its role?

A

bone morphogenetic protein (BMP)

TGFß

Main role is laying down extracellular matrix

150
Q

State the ways in which signals are turned off?

A
  1. Spontaneous breakdown
  2. Enzymatic breakdown
  3. Reuptake
  4. Receptor/ligand internalisation
151
Q

Tell me about Spontaneous breakdown, using the example of NO

A
  • NO is very labile (a free radical with an unpaired electron) and is converted to NO3- quickly and needs no catabolising enzyme
  • Hence it can’t move far from its site of production and has very local effects
  • Spontaneous and doesn’t require an enzyme
  • Localised effects
152
Q

Tell me the two forms of enzymatic breakdown that could occur?

A
  • Acetyl cholinesterase
  • Proteases
153
Q

Tell me about Acetyl cholinesterase break down

A

Acetyl Cholinesterase breaks down acetylcholine at the synapse. The enzyme is at high concentration (mostly membrane bound) and so there is only very local effect at the synapse which is short acting

154
Q

Tell me about Protease break down?

A

cleave peptide/ protein hormones (insulin, glucagon etc), these are often at lower concentrations and so produce longer term effects

155
Q

Tell me about reuptake and some examples

A

Many neurotransmitters are transferred back into the secreting cell

e.g. GABA, glycine, serotonin

156
Q

Tell me about receptor/ligand internalisation and some examples

A

Some ligands and their receptor are brought into the cell following binding via. Endocytosis

Ligand to be recycled or broken down

e.g. somatostatin and Luteinizing hormone.

157
Q

Breakdown/ uptake pathways are targets for pharmaceutical agents.

Name 2 agents?

A
  • Neostigmine
  • Fluoxetine
158
Q

Tell me the role of Neostigmine and what its used to treat

A

blocks acetylcholine esterase and so increases the effectiveness of acetylcholine

used to treat myasthenia gravis (autoimmune disease where body acts against the Ach receptors)

159
Q

Tell me about Fluoxetine and what its used to treat

A

Another name for it is Prozac

blocks serotonin uptake at the synapse, inhibits serotonin transporter

used to treat depression as the ligand is retained at the synapse for longer.

BIOL1013 (9 decks)

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