Cyclic AMP is formed from cytosolic ATP by the enzyme adenylyl cyclase
adenylyl cyclase is anchored in the plasma membrane with catalytic portion protruding into the cytosol
normally it is inactive until it binds to an activated G alpha subunit of a specific G protein such as Gs
when G protein linked receptor is coupled to Gs the binding of ligand stimulates the Gsa unit to release GDP and acquire a GTP
causes GTP-GSa to detach from the GSby subunits and bind to adenylyl cyclase
when binds to adenylyl cylcase the enzyme becomes active and converts ATP to cAMP
Gia inhibits the adenylyl cyclase
G proteins respond quickly to changes because they remain active only for short time before the G alpha subunit hydrolyzes GTP and converts to the inactive state
onces becomes inactive the adenylyl cyclase ceases to make cAMP
cAMP would remain elevated in the cell if it weren't for phosphodiesterase- degrades cAMP (further ensures that the signal transduction will be shut down)
cAMP important for many cellular events- glycogen degradation fatty acid production heart rate blood pressure, water reabsorption, bone resorption
cAMP has one main intracellular target- the enzyme protein kinase A
PKA phosphorylates by transferring a phosphate from ATP to a serene or threonine found within the target protein
cAMP regulates the activity of PKA by causing the detachment of its two regulatory subunits from its catalytic subunits
once catalytic submits are free PKA can catalyze the phosphorylation of various proteins in the cell
increase in cAMP in skeletal and liver cells the breakdown of glycogen is stimulated. increase in cardiac muscle strengthens heart contraction whereas the smooth muscles contraction is inhibited

	Erstellt von saranilsson47 vor etwa 10 Jahre

Cell and Molecular Final