Signal transduction pathways Flashcards

1
Q

endocrine

A

cell to blood to target cell

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2
Q

paracrine

A

cell to target cell

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3
Q

autocrine

A

cell to same cell

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4
Q

contact dependant

A

cell to cell by membrane attached proteins

requires direct contact

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5
Q

signal transduction

A

requires amplification of the signal within the cell to trigger the response
will require a system to slow/stop the amplification
faults here can lead to cancer

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6
Q

signal transduction pathways

A

4 types of mechanism:

  1. direct ligand gated channel
  2. G-protein-coupled
  3. tyrosine kinase-linked
  4. nuclear receptor super family
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7
Q

ligand gated channel

A

ion binds to receptor causing conformational change allowing influx into the cell through the channel
include:
uniporter
symporter
antiporter
ATPase dependant transport
also includes diffusion, facilitated transport and energy dependant transport

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8
Q

drug resistance ATPase

A

drug enters cell via diffusion, cell activates ATPase transport to remove drug from cell

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9
Q

G-protein-coupled

A

binding causes conformational shape change
can now bind to G-a subunit
triggers further change, causing dissociation of intracellular Go proteins which bind to, and cause a change to other transporter molecules
target of ~40% modern drugs

cAMP signal pathway:
messenger binds to receptor in the cellular membrane
causes change in the G-protein bound to the receptor
one sub-unit of the G-protein bins to adenylyl cyclase in the membrane
ATP arrives and is converted into cAMP

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10
Q

vasopressin

A

causes antidiuresis

single amino acid mutations in V2R can cause this ability to regulate water to be lost

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11
Q

tyrosine kinase-linked - Boron pg.111

includes several cytokines: IL-2,3,4,5,6 and more

A

there is a poir of receptors that hetero/homo-dimerise
GTP donates phosphate to activate intermediaries triggering a response
deficits in phosphatase will result in the ability to stop response signal being lost, since phosphate cannot be cleaved
homodimer - e.g. HER1 + HER1
very stable
heterodimer - e.g. HER1 + HER2
more unstable

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12
Q

hypoxia induced factors - von hippel lindau function

A

causes angiogenesis and proliferation
protective in the case of injury
e.g. diabetic retinopathy where process is disrupted

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13
Q

hypoxia induced factors - von hippel lindau function

A

causes angiogenesis and proliferation
protective in the case of injury
e.g. diabetic retinopathy where process is disrupted

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14
Q

VEGF - vascular endothelial growth factor

A

inhibited by thalidomide
? therapeutic use in haematological conditions
e.g. malignancy, retinopathy

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15
Q

VEGF - vascular endothelial growth factor

A

inhibited by thalidomide
? therapeutic use in haematological conditions
e.g. malignancy, retinopathy

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16
Q

thromboembolism risk anti-cancer medications

A

anti-cancer drugs often affect the tumour vis indirect effects as well as direct

17
Q

TNF

A

only activates death pathways within cells in cells with oxygen
in hypoxic conditions it causes proliferation and angiogenesis leading to growth

18
Q

TNF

A

only activates death pathways within cells in cells with oxygen
in hypoxic conditions e.g. tumours, it causes proliferation and angiogenesis leading to growth

19
Q

TNF

A

only activates death pathways within cells in cells with oxygen
in hypoxic conditions e.g. tumours, it causes proliferation and angiogenesis leading to growth
if the mets are hypoxic, and the rest of the surrounding tissue is oxic, can lead to damage to surrounding tissue and proliferation of the mets

20
Q

contact inhibition

A

often lost within cancer cells

21
Q

Tyrosine kinase receptors

A

2 signalling molecule bind to 2 adjacent receptor kinase proteins
this causes them to bind together - dimerisation
these are now activated
they are phosphorylated by 6 ATP (which become 6 ADP)
they are now able to activate inactive relat proteins within the cell