Lecture 2 Cell-derived signalling molecules Flashcards

Cell derived signalling

1
Q

What are the types of secretion routes for proteins?

A
  • classical pathway
  • transporter proteins
  • secretory vesicles (granules)
  • exosomes
  • microvesicles
  • shaving, with sheddase
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2
Q

How can the signals induce cell signalling in the target cells? (import of the signals into the cells)

A
  • direct import of proteins
  • receptor mediated signal transduction
  • receptor- mediated signal transduction with other peptides
  • vesicles fusion > fusion
  • receptor- mediated interaction > vesicle fusion > cargo release
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3
Q

What are the steps of neurotransmitter release?

A
  1. synaptic vesicles stored with neutrotransmitters in synapses
  2. depolarisation
    3.calcium gets in through channels
  3. calcium interacts with synapsin
  4. synapsin dissociates from vesicles
  5. snare proteins are activated(syntaxin and SNAP-25)
  6. SNARE complex forms with synaptobrevin
  7. membrane of vesicle fuse with the cell membrane
  8. NSF and SNAP disassemble SNARE complex
  9. vesicles can be recycled again.
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4
Q

What does Sarin do to the neurons?

A

Sarin fits on the enzyme acetylcholinesterase. By inhibiting this enzyme, acetylcholine will not be broken down and aggregate in the synapses. This will cause the muscle unable to relax.
Symptoms: shivering, foaming, fainting, inability to breath out.

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5
Q

How are RNA molecules secreted?

A
  • microvesicles
  • exosomes
  • lipoproteins
  • argonaite
    last two are carrier proteins
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6
Q

What types of extracellular RNAs are there?

A
  • messenger RNA
  • transfer RNA
  • microRNA (degrades the mRNA inside the cell also)
  • small- interfering RNA
  • long non-coding RNA
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7
Q

How can metastatic cancer break to barrier? ( e.g. the epithelial barrier)

A
  • they can secrete miRNA that interfere with ZO-1mRNA. This means that the epithelial barrier will be compromised an that the cancer can further metastasis.
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8
Q

What types of gasotransmitters are known currently?

A
  • Nitric oxide (NO)
  • Carbon monoxide (CO)
  • Hydrogen Sulphide (H2S)
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9
Q

What is the half life of each gasotransmitter?

A
  • NO = seconds
  • CO- minutes
  • H2S = seconds- minutes
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10
Q

What is the main function of NO as gasotransmitter?

A

NO can cause vasodilation through binding to guanylyl cyclase. THen GTP > cGMP which results in relaxation in the smooth muscle cell

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11
Q

Give a list of all the functions of NO.

A
  • LDL oxidation inhibition
  • msooth muscle cell proliferation inhibition
  • monocyte adhesion inhibition
  • platelet aggregation inhibition
  • superoxide radical elaboration inhibition
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12
Q

From what is CO produced?

A

From heme in the spleen

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13
Q

What is CO?

A

A gasotransmitter that can be vasodilatory, anti-thrombotic, anti-apoptotic and anti-inflammatory

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14
Q

What pathways can CO activate?

A
  • sGC
  • MAPK (p38)
  • Akt
  • NO-release, calcium dependant
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15
Q

CO and NO have a similar target molecule, what is it?

A

guanylate cyclase

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16
Q

What is the precursor of H2S?

A

methionine that becomes homocysteine > cysteine > H2S

17
Q

Why is specifically cysteine needed for H2S.

A

Cysteine is the only amino acid that contains sulphur.

18
Q

What is the function of H2S?

A
  • angiogenesis
  • vasodilation
  • lower mitochondrial respiration
  • anti-inflammation
  • anti-oxidation
19
Q

What are the classes of lipid derivatives?

A
  • eicosanoids
  • phosphoinositides
  • sphingolipids
  • fatty acids
  • cholesterol derived molecules (hormones)
20
Q

What are the functions of lipid-derivatives?

A
  • activators of G-protein coupled receptors
  • activators of nuclear receptors
21
Q

What are the 4 main classes of hormones?

A
  • amino hormones
  • peptides
  • eicosanoids (inflammation , blood pressure etc. )
  • steroids ( sex hormones, blood sugar, immune suppression etc. )
22
Q
A