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Cell Communication Flashcards

1
Q

What is contact dependent communication?

A

Adjacent cells with physical contact and interaction

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2
Q

What is an example of contact-dependent communication?

A

The Notch pathway

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3
Q

Describe paracrine communication

A

A local mediator is sent out and received by surrounding cells, migrating proteins to interact with receptors

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4
Q

Describe Endocrine communication

A

The production of hormones travelling through the bloodstream and cells receive a signal by expressing a receptor

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5
Q

Give two examples of signals

A

Adrenaline and Pheromones

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6
Q

Give two ways cells can respond to signalling

A
  1. Changes to cytoskeleton as a direct response to signalling
  2. Changes to gene expression to produce certain enzymes
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7
Q

What is a Morphogen gradien?

A

Morphogen secreted and forms a gradient of concentration which leads to different levels of expression in tissues, molecules can be completely different depending on the dose

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8
Q

How can cells respond to a signal? (3)

A
  1. Changing the structure of an existing protein (ion channel)
  2. Changing the post translational modification (phosphorylation)
  3. Changing the protein levels via gene expression
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9
Q

What happens during Chronic Myeloid Leukaemia?

A
  • BCR-Abl fusion protein causes sustained tyrosine kinase expression (more phosphorylation) by the BcR promoter region, more growth of white blood cells
  • Treated with an abl kinase inhibitor
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10
Q

What is positive and negative feedback in terms of signalling?

A

Positive= Product of signal reinforces original signal
Negative = Product of signal inhibits original signal

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11
Q

How does the body deal with fast responses requiring rapid turnover of the effector?

A

Proteins are always there they are just phosphorylated (e.g.) when needed
Saves making proteins and destroying them just in case you need them

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12
Q

What are the main types of kinases?

A

Serine/Theonine kinases and tyrosine kinases

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13
Q

Which two parts of the brain are involved in linking the neuronal and endocrinological systems?

A

Hypothalamus and pituitary

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14
Q

What special properties do steroid hormones have?

A

They have hydrophilic and hydrophobic properties meaning they can penetrate through all membranes including the blood brain barrier

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15
Q

What are the receptors for steroid hormones + describe the structure?

A
  • Proteins/Transcription factors
  • Have a DNA binding domain which encodes zinc fingers that contain cystine residues and zinc forming a loop structure which is able to access the major groove of the DNA double helix
  • Ligand binds to receptor causing conformational change and the steroid hormone becomes locked in the binding pocket
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16
Q

What important hormones is cholesterol a precursor for?

A

Cortisol and testosterone

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17
Q

What are the two classes steroid hormones are grouped into?

A
  1. Sex steroids
  2. Corticosteroids
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18
Q

What are the 5 subtypes the two classes are grouped into?

A

Sex steroids:
- Androgens
- Oestrogens
- Progestogens

Corticosteroids:
- glucocorticoids
- mineralocorticoids

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19
Q

Why are these hormones known as nuclear hormone receptors?

A

They are present in the nucleus where transcription factors work

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20
Q

How does an inactive nuclear receptor become an active nuclear receptor

A

Inactive:
- The inactive receptor is bound to an inhibitory protein
Active:
- Ligand binding causes conformational change which causes the inhibitory protein to disassociate from the receptor
- Receptor ligand complex can now bind to DNA sequences at the DNA binding domain, acts as a promoter to target genes
- Ligand binding domain shuts tight around the ligand and a coactivator protein joins to initiate gene transcription

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21
Q

What do primary response proteins do?

A
  • Made through transcription of the Receptor ligand binding
  • Turn off primary response genes
  • Turn on secondary response genes to initiate a cascade
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22
Q

What do corticotropin releasing hormones do?

A
  • Stimulate pituitary gland
  • Pituitary releases ACTH
  • ACTH binds to adrenal gland and triggers production of cortisol
23
Q

What is cortisol and what is it used for in the body?

A
  • Cortisol is a glucocorticoid class steroid hormone
  • released in response to stress and reduced blood sugar levels
  • Affects metabolism, immune system, electrolyte balance, memory
24
Q

What are glucocorticoids useful for?

A

They are immunosuppressants and anti-inflammatory agents

25
What happens in the body during Addisons disease?
- Body is not making cortisol - Lack of ACTH - To see if they have secondary adrenal insufficiency you give the patient ACTH and see if they can produce cortisol - Depression, flu-like symptoms, nausea, weight loss, body can go in shock if something bad happens
26
What is Cushing's syndrome?
- Increased levels of cortisol caused by adenoma growing in the pituitary gland leading to increased ACTH production - Can also be caused by long term steroid abuse
27
What is type 1 diabetes?
- When your body stops being able to deal with the glucose that you take in through your diet - Caused by destruction of the beta cells that make insulin due to an auto-immune attack
28
Describe the structure of insulin receptors
Heterotetrameric protein complexes 2 alpha 2 beta The two beta are tyrosine kinase domains
29
What does ligand binding to the insulin receptor do?
Moves the two kinases closer together
30
What are the three major biochemical steps in insulin signalling?
1. Tyrosine phosphorylation of the receptor and insulin receptor substrates 2. Activation of the lipid kinase PI3K 3. Activation of multiple serine/threonine kinases (most important is AKT)
31
What is hypo-glycemia?
Excess insulin leading to too little blood sugar - Can lead to unconsciousness and death - Poor brain circulation, periodontal disease, blindness etc.
32
What is type 2 diabetes?
- Dysregulation of carb, lipid and protein metabolism - Impaired insulin secretion, insulin resistance or both
33
What is the treatment for Type II diabetes and how does it work?
Metformin which inhibits mitochondrial activity reducing production of mitochondrial ATP which activates AMPK which is an enzyme involved in glucose metabolism
34
Describe the extracellular domain of trans-membrane receptor tyrosine kinases
- Hydrophilic -Interacts with ligand - Often contains things such as immunoglobulin, cysteine rich regions, epidermal growth factors etc.
35
Describe the transmembrane segment of transmembrane receptor tyrosine kinases
- 20-25 amino acids - Almost always helical stabilised with the acid chains of the lipid bilayer
36
Describe the intracellular domain of the transmembrane receptor tyrosine kinases
- Hydrophobic - Interacts with downstream signalling machinery - Involves a tyrosine kinase domain
37
What is a signal-peptide?
Something the genes encidoing transmembrane proteins include which directs the newly synthesises protein to the endoplasmic reticulum
38
How is information transferred from the outside to the inside of a transmembrane molecule?
1. conformational changes to multi-pass transmembrane receptors which are then often associated with G-proteins 2. Dimerization/multimerization of single-pass transmembrane receptors (rotating two molecules causing them to face each other and then bind)
39
What ways can transmembrane receptors be activated?
- Dimerization of extracellular ligand (receptors are brought together and activate eachother) - Monomeric ligand with receptor binding sites ligands that induces changes in the receptor like their affinity for one another - Enzymatic activity: kinases, phosphorylating each other because they cant phosphorylate themselves
40
Where was the downstream Ras pathway first identified?
Drosophila flies
41
Describe the drosophila eye structure
- 800 ommatidium which radiate out at slightly different angles - Each contains a range of photoreceptor cells - If you were to take a cross section you would see raptomeres (?) which have rhodopsin in them and translate light into neuronal impulse
42
How did the drosophila eye structure derive?
- Imaginal disc in larva - R8 cells formed in morphogenetic furrow are the foundation cells - Spaced by notch signalling and positive feedback loops - Once R8 cells are spaced out, cells are recruited (R2,5,3 etc) (This requires the ras pathway..) - Ended up with a pathway where ligands are presented by R8 cells and then so on
43
What is the Ras Pathway?
- Ligand binds to transmembrane receptor and pulls two together - Phosphorylation of tyrosine happens leaving a phosphorylated receptor ligand complex - Grb2 then binds it has a SH2 domain which recognises phosphorylated tyrosine residues - SOS (Guanosine nucleotide exchange factor ) binds to Grb2 - SOS helps RAS (G-protein) exchange its GDP for GTP (activating RAS protein) - RAS interacts with RAF and then MEK, phosphorylating it and activating it - MEK then activates and phosphorylates ERK which then translocates into the nucleus - Phosphorylated ERK interacts with transcription factors allowing gene transcription to happen - The genes transcribed are genes that control cell growth and division (proliferation)
44
How is the RAS pathway negatively regulated?
- Before RAF can be activated the N-terminal, the 14-3-3 protein and a phosphate group needs to eb removed - Erk negatively phosphorylates SOS to prevent grb2 binding
45
How are small GTPases similar and different from G-proteins associated with GPCRs?
- They aren't transmembrane, just membrane tethered - Both regulated by GEFs and GAPs and activated by being bound to a GTP nucleotide
46
What is the small GTPase 'rho' responsible for?
- Cytoskeletal movement - Cell morphology movement - Macrophage activity - Recycling exocytosis
47
Which group of cancers have the RAF pathway activated?
- Melanomas - Signalling activated in 80% of melanomas - Most problems occurring with kinase activating loop
48
What has been used to treat malignant melanomas and why didn't it work?
- BRAF inhibitors - Didn't work because not every mutant BRAF was targeted so it came back with more resistance aswell
49
How are melanomas more commonly treated now?
- BRAF inhibitors selectively for mutant MRAF - BRAF and MEK inhibitors to stop further downstream signalling if some of the BRAF inhibitors do not target all
50
Describe the Jak-Stat Pathway
- Pathway starts with activation of membrane bound cytokine receptor - Cytokine receptors do not harbour kinase domains for tyrosine residues - When cytokine binds and the receptor is activated it recruits intracellular kinases of the JAK family to its cytoplasmic domains - JAKS phosphorylate tyrosine residues of receptor - STAT proteins carry SH2 domains and bind to the phosphorylated residue - STATS are then phosphorylated and dissociate - PSTATS enter the nucleus and activate transcription of many target genes
51
How many STATS and JAKs are there?
7 STATS 4 JAKS
52
What is the JAK/STAT pathway important for?
- Inflammation and immunity - Haematopoiesis (proliferation of blood cells)
53
What is myeloproliferative neoplasms?
- Most common mutation in JAk2 - Over proliferation of red blood cells - Jak2 is veryyyy negatively regulated so any mutation which increases is harmful (normal expression is 1%)
54

Advanced Molecular (13 decks)

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