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In the insulin receptor (IR), essentially the $\alpha$ subunit is responsible for binding and the $\beta$ subunit is responsible for enzymatic activity. In some forms of diabetes (primarily diabetes mellitus), enzymatic activity in the insulin receptor (IR) is abolished due to a mutation in the $\beta$ subunit.

How is the cell's response to insulin affected by this mutation?


The mutation affects the K$_M$ of insulin, requiring higher concentrations of insulin to achieve the same effect as a 'normal' dose.


Insulin is phosphorylated upon binding.


Tyrosine kinase activity is inhibited, preventing autophosphorylation or other phosphorylation reactions.


The G$_\alpha$ subunit is prevented from dissociation preventing the formation of cAMP.


Because the mutation is in the $\beta$ subunit, there is no effect.

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