get help please with this question? Two mutations have occurred to proteins within the glucagon signaling pathway: A) The glucagon receptor has a mutation. This mutation causes this GPCR to always have a conformation that will induce nucleotide exchange for any associated heterotrimeric G proteins, even without glucagon binding to the receptor. B) The alpha subunit of the heterotrimeric G protein has a mutation. This mutation causes the Gαarginine finger to always be in a position to properly order the catalytic residues within the Gαsubunit to promote catalysis. Question: What will the combined effect of both mutations be on the signaling pathway and what is the mechanistic reason for this effect
Two mutations have occurred to proteins within the glucagon signaling pathway:
A) The glucagon receptor has a mutation. This mutation causes this GPCR to always have a conformation that will induce
B) The alpha subunit of the heterotrimeric G protein has a mutation. This mutation causes the Gαarginine finger to always be in a position to properly order the catalytic residues within the Gαsubunit to promote catalysis.
Question: What will the combined effect of both mutations be on the signaling pathway and what is the mechanistic reason for this effect?
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Upon activation by a ligand, the GPCR undergoes a conformational change and then activate the G proteins by promoting the exchange of GDP/GTP associated with the Gα subunit.
This leads to the dissociation of Gβ/Gγ dimer from Gα. Both these moieties then become free to act upon their downstream effectors.
The GPCR is turned on due to mutation and thus dissociation of Gβ/Gγ dimer from Gα is unstoppable.
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