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Y3 Signalling > Single Pass Receptors > Flashcards

Single Pass Receptors Flashcards

1
Q

What is a catalytic receptor?

A

Receptor with enzymatic activity

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2
Q

What is a non-catalytic receptor?

A

Receptor that has to couple with other proteins for enzymatic activity

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3
Q

Describe TGF-β pathway

A
  1. Ligand binds to type II receptor which recruits and phosphorylates a type I receptor
  2. Serine kinases phosphorylate SMADs
  3. Phosphorylation reveals the SMAD NLS so SMADs move to the nucleus and act as a transcription factor
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4
Q

What do TGF-β downstream genes affect?

A

Immune cell regulation
Maintaining undifferentiated stem cells via Oct4
Common in cancer, e.g bone morphogenic protein (BMP strenghens bone after fractures and maintain undifferentiated stem cell states)

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5
Q

What happens when TGF-β signalling is lost?

A

Cells become resistant to growth inhibition
Most pancreatic cancers have a deletion in the SMAD4 gene which prevents cell cycle inhibitors activating
Retinoblastoma, colon and gastric cancer are unresponsive to the inhibition

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6
Q

What happens when TGF-β is overstimulated?

A

TGF-β signalling induces SnoN and Ski. These are elevated in cancers.
These bind SMAD4 and phosphorylated SMAD3, sequestering transcriptional activity and preventing long term hormone action

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7
Q

Describe what happens when a ligand binds to a RTK

A
  1. Ligand binding pushes out a loop that allows dimerisation
  2. The cytosolic Tyrs are trans-phosphorylated
  3. Grb2 binds phosphorylated RTK and SOS binds to the SH3 domain
  4. Ras-GTP binds and regulates kinase cascades
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8
Q

What is the kinase cascade that SOS causes Ras to activate?

A

MAPKKK
MAPKK
MAPK
Transcription factor

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9
Q

How is SOS localised to the cell membrane?

A

Farnesyl group

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10
Q

How do Ras isoforms differ?

A

Localised by different hydrocarbons on different surfaces.
K-ras has a farnesyl chain and joins to plasma membrane
N- and H-Ras have palmitoyl chains. These can join to plasma membrane or golgi

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11
Q

What pathway inhibits apoptosis?

A
  1. PLC (activated by Ras-GTP or Gq) converts PIP2 to IP3 and DAG
  2. PI3K converts IP3 to PIP3
  3. This activates PKB/Akt, phosphorylating bad
  4. Phosphorylated bad inhibits Caspase and therefore apoptosis
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12
Q

What EGF is prominent in cancers?

A

HER2 has an active loop configuration that binds HER1, 3 or 4, activating proliferation
Too much HER2 makes signalling pathways less regulated, leading to lower cancer survival

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13
Q

How does herceptin work?

A

Blocks HER2 dimerisation

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14
Q

How is Abl kinase autoinhibited?

A

Its active site is held open
(think The Weeknd singing with his mouth open)
SH2 is docked to the kinase and SH3 is sequestered

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15
Q

How is Src kinase activated?

A
  1. C-terminal Tyr or SH2/SH3 is dephosphorylated
  2. SH2 binds to a better pY sequence
  3. SH3 binds to a better proline-rich sequence, activating it
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16
Q

How is Src kinase inhibited?

A
  1. SH2 binds to a pY near the C-terminus
  2. SH3 binds to a proline-rich sequence that locks it shut
  3. Active site is distorted
17
Q

How can mutations in Abl and Src kinase cause cancers?

A

SH3 not being able to inhibit them
Proline-rich sequence not binding at all

18
Q

How does Grb2 autoinhibit?

A

Its domains stick to each other

19
Q

What does excessive TNFα receptor cause?

A

Excessive inflammation in autoimmune conditions such as psoriasis, rheumatoid arthritis and type I diabetes

20
Q

Outline how an insulin receptor is activated

A
  1. Insulin binding closes the extracellular domain, causing CAM shafts to move the A-loops so they phosphorylate the receptor
  2. Phosphorylated receptor binds to IRS1 (scaffold protein)
  3. Grb2 binds to phosphorylated domain with its SH2 domain
  4. SOS can bind to this and signal via PI3K for Akt/PKB and PKC5 cascades
21
Q

Describe cytokine receptor activation

A
  1. Cytokine binds to a receptor
  2. They move in close enough proximity for JAKs to phosphorylate each other
  3. Phosphorylated JAKs phosphorylate Tyr on receptors
  4. STAT binds phosphotyrosines via SH2
  5. JAK phosphorylates STAT, causing STAT to dissociate from the receptor
  6. STAT forms a dimer and acts as a transcription factor with the help of DNA binding protein

Y3 Signalling (6 decks)

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