What is the effect of INSR phosphorylation on IRS-1?

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Multiple Choice

What is the effect of INSR phosphorylation on IRS-1?

Explanation:
The phosphorylation of the insulin receptor substrate 1 (IRS-1) by the insulin receptor (INSR) plays a critical role in insulin signaling pathways. When the insulin receptor is activated by insulin binding, it undergoes autophosphorylation and subsequently phosphorylates IRS-1. This phosphorylation event is crucial because it allows IRS-1 to interact with various signaling molecules, leading to a cascade of downstream signaling events. These downstream events typically involve the activation of PI3-kinase, which subsequently promotes lipid and glucose metabolism, among other functions in the cell. The process instigated by IRS-1 phosphorylation ultimately results in various cellular responses such as glucose uptake and lipid synthesis, but the key factor here is that the phosphorylation directly triggers a cascade of kinase activation that propagates the insulin signaling pathway. Thus, the phosphorylation of IRS-1 by INSR does more than just initiate a single reaction; it sets off a series of events that are essential for mediating the effects of insulin in the body. This is why the correct response focuses on the initiation of a kinase cascade as a direct consequence of INSR phosphorylation of IRS-1.

The phosphorylation of the insulin receptor substrate 1 (IRS-1) by the insulin receptor (INSR) plays a critical role in insulin signaling pathways. When the insulin receptor is activated by insulin binding, it undergoes autophosphorylation and subsequently phosphorylates IRS-1. This phosphorylation event is crucial because it allows IRS-1 to interact with various signaling molecules, leading to a cascade of downstream signaling events.

These downstream events typically involve the activation of PI3-kinase, which subsequently promotes lipid and glucose metabolism, among other functions in the cell. The process instigated by IRS-1 phosphorylation ultimately results in various cellular responses such as glucose uptake and lipid synthesis, but the key factor here is that the phosphorylation directly triggers a cascade of kinase activation that propagates the insulin signaling pathway.

Thus, the phosphorylation of IRS-1 by INSR does more than just initiate a single reaction; it sets off a series of events that are essential for mediating the effects of insulin in the body. This is why the correct response focuses on the initiation of a kinase cascade as a direct consequence of INSR phosphorylation of IRS-1.

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