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ICS > Receptors > Flashcards

Receptors Flashcards

1
Q

what are the 4 main types of receptors?

A
  • steroid
  • G coupled receptors
  • Ion channels
  • enzyme linked
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2
Q

what is a G protein coupled receptor?

A
  • single polypeptides that are folded into globular shape and are embedded in the cells plasma memembrane
  • 7 segments that span the width of the membrane
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3
Q

what is an alternative name for G protein coupled receptors?

A

seven-transmembrane receptors

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4
Q

what are G proteins?

A

specialised proteins that have the ability to bind to the nucleotides GTP (guanosine triphosphate) and GDP

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5
Q

what does heterotrimeric mean?

A

3 subunits (alpha, beta and gamma)

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6
Q

when the G protein alpha binds to the subunits GTP of GDP, which is active and which is inactive?

A

GTP= active and GDP=inactive

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7
Q

G protein- what happens to the GDP (which is attached to the alpha subunit) when there is a signal?

A

The GTP molecule physically replaces the GDP

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8
Q

G protein-what happens to the subunits when there is a signal?

A
  • dissociate into 2 parts (alpha and gamma + beta together) … GTP bound alpha subunit and a beta gamma dimer
  • they remain anchored to the plasma membrane
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9
Q

what makes the GPCR remain active?

A

the GTP being bound to the alpha subunit

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10
Q

what hydrolyses the GTP back to GDP?

A

GTPase

-then once again a heterotrimer and an inactive GPCR

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11
Q

what is the second messenger in the GPCR?

A

cyclic AMP

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12
Q

what is cAMP synthesised from?

A

ATP by the adenylate cyclase

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13
Q

in the GPCR if there is lots of adenylate cyclase and not much cyclic AMP what happens?

A

you get a high level of cAMP

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14
Q

what does the cAMP act on?

A

kinases, which then act on transcription factors and other targets to cause transcription of certain genes

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15
Q

what do kinases catalyse?

A

phosphorylation. ..
- addition of phosphate groups to specific serine, threonine or tyrosine side chains
- in the GPCR phosphorylatiion of transcription factors at the start of a gene

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16
Q

how do kinases case the release of Ca2+?

A

Ca2+ is stored in the ER, and then the phosphorylation of certain molecules causes the ligand gated ion chanel to release Ca2+P

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17
Q

where are steroid molecules derived from?

A

from cholesterol molecules

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18
Q

what are the characters of steroid molecules?

A

lipid soluble, hydrophobic, so they go straight into the cytoplasm

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19
Q

how do steroids influence gene transcription?

A

the steroid and receptor move into the nucleus and act as transcription factor that are required for promoting the formation of mRNA

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20
Q

How do steroid receptors work?

A

the steroid moves through the membrane into the cytoplasm, where it meets the receptor, when the receptor and the steroid join they then move into the nucleus together and affect transcription

21
Q

how does testosterone regulate its own production?

A

dec. GnRH, decrease in FSH and LH… the hypothalamus controls the release of GnRH depending on the levels of testosterone
negative feedback

22
Q

How do ligand gated ion channels work?

A

They open when a ligand binds and allows ions to flow down a gradient

23
Q

what are examples or a ligand gated ion channels?

A

serotonin and GABA receptors

24
Q

what do phosophotases do?

A

remove phosphate groups

25
Q

what do kinases and phosphotases regulate?

A

-activity-
localisation
-stability of target proteins

26
Q

what is an example of an enzyme linked receptor and itsligand?

A

VEGF- is the ligand that activates the receptor
causes a phosphorylation, of its neibour …
-localise a GEF (SOS)causes GRb2 and SOS to activate Ras to bring GTP and which binds activates other kinases (dominoes) to activate transcription factors

27
Q

what are CDKs and what do they do?

A

cyclin dependent kinases that regulate the cell cycle

28
Q

where are the checkpoints in th cell cycle?

A
  • between G1 and S

- between G2 and S

29
Q

Cells respond to signals by modulating the activity of..?

A

Genes, Ribosomes, enzymes and the cytoskeleton

30
Q

Turning genes on and off is important because?

A

it changes protein expression

31
Q

What would you analyse to see which genes are up regulated and down regulated by testosterone?

A

-RNA and proteins

32
Q

Where would you find the N terminus on a GPCR?

A

at the start of the protein. on the very top

33
Q

What does a GPRC look like?

A

7 spanning transmembrane proteins… spans the membrane from outside to inside

34
Q

what proportion of your genes code for GPCR?

A

1/20

approx. 1000 genes

35
Q

How do we know how many different GPCR humans have?

A

genome sequencing

36
Q

what would you expect to happen if you added GaS specific GTPase inhibitor to a leydig cell?… why?

A
  • Increase in testosterone production
  • Galpha proteins contain intrinsic GTPase activity
  • G-proteins are bound to GTP and off when bound to GTP
  • GTPase turns G protein off
  • if GTPase inhibited, keeps GaS on and generating signals to produce testosterone
37
Q

What is the function of a second messenger?

A

to amplify the signal

38
Q

What do second messengers do?

A

they are very small molecules that are produced quickly and can activate lots of target molecule

39
Q

What effect do kinases have on their target proteins?

A

-stimulate activity
(can also repress the activity of things)
-Provide a binding site for other proteins
-trigger degradation
-change its charge

40
Q

What type of receptor do photoreceptors in the retina use?

A

GCPR

41
Q

Explain the mechanism of the GCPR in the retina.

A
  • photoreceptor cells in the retina detect light using rhodopsin coupled to GaT
  • cell membranes are impermeable to ions (e.g. Na+)- must pass through protein channels to move in and out of cells
  • absence of light cGMP predominates in the cytoplasm keeping the Na+ channel open
  • photon excites rhodopsin, activates GaT… cGMP is linearised and the channel closes… difference across membrane increased-nerve impulse
42
Q

what are the first and second messengers in the GCPR in th retina?

A

1st messenger- photon

2nd-cGMP (or lack of)

43
Q

what is required for a GCPR to work?

A

cAMP or cGMP depending on the specific system, required to turn the signal on and off

44
Q

mantra related with receptors?

A

signal receptor transduction cell response

45
Q

an example of a disease where there are too many receptor Tyrosine kinases?.. how could you treat?

A

breast cancer

-kinase inhibitors, antibodies

46
Q

Receptor tyrosine kinases

A
  • ligand binds to receptor-
  • kinases phosphorylate one another
  • Grb2 and SOS are activated (phosphorylated)
  • these then activate Ras which causes a MAP kinase cascade
  • the effector if then phosphorylated and moves into the nucleus to start transcription
47
Q

If Ras had a mutation that wipes out GTPase activity completely what would happen in the cell?

A

-Ras would be locked in an on state, signalling for the cell to divide, mutation found in many cancers… need to inhibit Ras effector e.g. the MAP kinase pathway or target transcription factors

48
Q

What is Hypoxia?

A

low oxygen supply

49
Q

What happens to HIF during low oxygen levels?

A
  • not degraded

- so activates specific genes which lead to the production of proteins that deal with low oxygen levels

ICS (11 decks)

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