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Advanced Molecular > Cell Communication > Flashcards

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
Q

What happens in the body during Addisons disease?

A
  • 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
Q

What is Cushing’s syndrome?

A
  • 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
Q

What is type 1 diabetes?

A
  • 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
Q

Describe the structure of insulin receptors

A

Heterotetrameric protein complexes
2 alpha 2 beta
The two beta are tyrosine kinase domains

29
Q

What does ligand binding to the insulin receptor do?

A

Moves the two kinases closer together

30
Q

What are the three major biochemical steps in insulin signalling?

A
  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
Q

What is hypo-glycemia?

A

Excess insulin leading to too little blood sugar
- Can lead to unconsciousness and death
- Poor brain circulation, periodontal disease, blindness etc.

32
Q

What is type 2 diabetes?

A
  • Dysregulation of carb, lipid and protein metabolism
  • Impaired insulin secretion, insulin resistance or both
33
Q

What is the treatment for Type II diabetes and how does it work?

A

Metformin which inhibits mitochondrial activity reducing production of mitochondrial ATP which activates AMPK which is an enzyme involved in glucose metabolism

34
Q

Describe the extracellular domain of trans-membrane receptor tyrosine kinases

A
  • Hydrophilic
    -Interacts with ligand
  • Often contains things such as immunoglobulin, cysteine rich regions, epidermal growth factors etc.
35
Q

Describe the transmembrane segment of transmembrane receptor tyrosine kinases

A
  • 20-25 amino acids
  • Almost always helical stabilised with the acid chains of the lipid bilayer
36
Q

Describe the intracellular domain of the transmembrane receptor tyrosine kinases

A
  • Hydrophobic
  • Interacts with downstream signalling machinery
  • Involves a tyrosine kinase domain
37
Q

What is a signal-peptide?

A

Something the genes encidoing transmembrane proteins include which directs the newly synthesises protein to the endoplasmic reticulum

38
Q

How is information transferred from the outside to the inside of a transmembrane molecule?

A
  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
Q

What ways can transmembrane receptors be activated?

A
  • 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
Q

Where was the downstream Ras pathway first identified?

A

Drosophila flies

41
Q

Describe the drosophila eye structure

A
  • 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
Q

How did the drosophila eye structure derive?

A
  • 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
Q

What is the Ras Pathway?

A
  • 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
Q

How is the RAS pathway negatively regulated?

A
  • 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
Q

How are small GTPases similar and different from G-proteins associated with GPCRs?

A
  • They aren’t transmembrane, just membrane tethered
  • Both regulated by GEFs and GAPs and activated by being bound to a GTP nucleotide
46
Q

What is the small GTPase ‘rho’ responsible for?

A
  • Cytoskeletal movement
  • Cell morphology movement
  • Macrophage activity
  • Recycling exocytosis
47
Q

Which group of cancers have the RAF pathway activated?

A
  • Melanomas
  • Signalling activated in 80% of melanomas
  • Most problems occurring with kinase activating loop
48
Q

What has been used to treat malignant melanomas and why didn’t it work?

A
  • BRAF inhibitors
  • Didn’t work because not every mutant BRAF was targeted so it came back with more resistance aswell
49
Q

How are melanomas more commonly treated now?

A
  • 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
Q

Describe the Jak-Stat Pathway

A
  • 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
Q

How many STATS and JAKs are there?

A

7 STATS
4 JAKS

52
Q

What is the JAK/STAT pathway important for?

A
  • Inflammation and immunity
  • Haematopoiesis (proliferation of blood cells)
53
Q

What is myeloproliferative neoplasms?

A
  • 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
Q
A

Advanced Molecular (13 decks)

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