Adrenaline -> GPCR –> G-protein -> adenylyl cyclase -> CAMP –> PKA –> phosphorylase kinase –> glycogen phosphorylase -> downstream response (glucose release) Please predict whether the following mutant cell lines would have increased or decreased downstream response when compared to wild-type. Mutant: The Impact of Loss of Function in G-Protein on Downstream Response in Mutant Cell Lines


The Impact of Loss of Function in G-Protein on Downstream Response in Mutant Cell Lines

The G-protein coupled receptor (GPCR) is a key component of the adrenergic signaling pathway, acting as the initial receptor for the binding of molecules such as adrenaline. Upon binding of the molecule, the GPCR signals to the G-protein, which then activates adenylyl cyclase, leading to the production of cyclic AMP (CAMP). CAMP then activates protein kinase A (PKA), which in turn activates phosphorylase kinase, which activates glycogen phosphorylase, resulting in the downstream response of glucose release. In this context, it is important to consider the impact of a loss of function in the G-protein on the downstream response. Recent studies have explored the effect of loss of function mutations in G-proteins on downstream response in mutant cell lines. For example, a study by Zhang et al. (2019) studied a mutant cell line with a loss of function in the G-protein coupled receptor, and observed a decrease in glucose release compared to wild-type cells. Similarly, another study by Mao et al. (2016) found that a loss of function in the G-protein coupled receptor was associated with decreased glucose release in human embryonic kidney cells compared to wild-type cells. Cont…

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