Cell signalling revision
G-protein coupled receptor
There is no right way to start this process as it’s in a loop
1. Ligand binds to the extracellular binding site
The process starts when a ligand (e.g., a hormone or neurotransmitter)
binds to the GPCR on the cell surface.
2. The GPCR changes its conformation
Ligand binding causes a conformational change in the GPCR, which is
necessary for activating the G-protein.
3. GDP is replaced by GTP
The interaction between the GPCR and the G-protein causes the exchange
of GDP for GTP on the Gα subunit, activating it.
4. The G-protein dissociates from the GPCR
Once GTP binds to the Gα subunit, the G-protein dissociates from the
GPCR.
5. G-protein binds to adenylate cyclase
The activated Gα-GTP subunit then interacts with adenylate cyclase, an
enzyme that catalyses the conversion of ATP to cAMP.
6. Adenylyl cyclase is allosterically activated
The binding of Gα-GTP to adenylate cyclase activates it, leading to an
increase in cAMP production.
7. cAMP is produced
Activated adenylate cyclase generates cAMP, which acts as a second
messenger in the cell.
8. G-protein spontaneously reverts to its inactive (GDP-bound)
form
After the signalling event, GTP is hydrolysed to GDP by the Gα subunit,
inactivating the G-protein and returning it to its resting state.
9. Gsα - GPCR binding is stabilized by Gsβ/Gsγ binding
The Gβ and Gγ subunits of the G-protein help stabilize the interaction
between Gsα and the GPCR.
10. G-protein binds to GPCR
The conformational change in the GPCR enables it to interact with the G-
protein (Gs in this case).
G-protein coupled receptor
There is no right way to start this process as it’s in a loop
1. Ligand binds to the extracellular binding site
The process starts when a ligand (e.g., a hormone or neurotransmitter)
binds to the GPCR on the cell surface.
2. The GPCR changes its conformation
Ligand binding causes a conformational change in the GPCR, which is
necessary for activating the G-protein.
3. GDP is replaced by GTP
The interaction between the GPCR and the G-protein causes the exchange
of GDP for GTP on the Gα subunit, activating it.
4. The G-protein dissociates from the GPCR
Once GTP binds to the Gα subunit, the G-protein dissociates from the
GPCR.
5. G-protein binds to adenylate cyclase
The activated Gα-GTP subunit then interacts with adenylate cyclase, an
enzyme that catalyses the conversion of ATP to cAMP.
6. Adenylyl cyclase is allosterically activated
The binding of Gα-GTP to adenylate cyclase activates it, leading to an
increase in cAMP production.
7. cAMP is produced
Activated adenylate cyclase generates cAMP, which acts as a second
messenger in the cell.
8. G-protein spontaneously reverts to its inactive (GDP-bound)
form
After the signalling event, GTP is hydrolysed to GDP by the Gα subunit,
inactivating the G-protein and returning it to its resting state.
9. Gsα - GPCR binding is stabilized by Gsβ/Gsγ binding
The Gβ and Gγ subunits of the G-protein help stabilize the interaction
between Gsα and the GPCR.
10. G-protein binds to GPCR
The conformational change in the GPCR enables it to interact with the G-
protein (Gs in this case).
