Any protein in the cytosol can dock on a receptor phosphotyrosine.
Circle one: True False
Why must a receptor tyrosine kinase pair up before it can signal?
- Binding alone switches one receptor on and starts the whole cascade firing at once
- Pairing only cleans up extra receptors
- Single growth factor receptors are inactive; only the dimer can cross-phosphorylate
What does autophosphorylation build on the receptor?
- Docking sites for specific adaptor proteins
- Second messengers flooding the cytosol at once
- New ligands for neighbouring receptors nearby
What does the phosphorylation cascade achieve?
- It slows the signal so the resting cell can fully recover afterwards
- It removes the need for any ligand at all
- It turns one active receptor into a flood of active kinases
How does RTK signalling differ from GPCR signalling?
- RTKs use G proteins while GPCRs phosphorylate themselves instead
- GPCRs use G proteins; RTKs dock adaptors directly
- Both use identical relays with different names
A mutant receptor dimerises without any ligand present. What happens?
- It signals nonstop, as if growth factor were always present
- It stays completely silent, since no ligand ever arrived to bind it
- It switches to G protein signalling instead
A drug covers the phosphotyrosine docks but pairing and phosphates stay normal, so the cascade still starts. True or false?
Circle one: True False
Theo says binding alone switches the receptor on and pairing just follows. True or false?
Circle one: True False