When insulin binds to its receptor, a conformational change occurs that results in auto phosphorylation of the receptor on a specific Tyr residues. In the next step of the signaling pathway, an adaptor protein called IRS-1(insulin receptor substrate-1) docks with the phosphorylated receptor. This step is essential for the downstream activation of several kinases including Alk, also known as protein B as well as protein C kinase and GSK-3. Protein kinase 3 is involved in mobilizing GLUT 4 glucose transporters to the plasma membrane and GSK-3 phosphorylates glycogen sunthase. What would be the effects of a mammalian organism over expressing IRS-1 were also deficient in muscle GAK-3? Would this deficiency be lethal ?
When insulin binds to its receptor, a conformational change occurs that results in auto phosphorylation of the receptor on a specific Tyr residues. In the next step of the signaling pathway, an adaptor protein called IRS-1(insulin receptor substrate-1) docks with the phosphorylated receptor. This step is essential for the downstream activation of several kinases including Alk, also known as protein B as well as protein C kinase and GSK-3. Protein kinase 3 is involved in mobilizing GLUT 4 glucose transporters to the plasma membrane and GSK-3 phosphorylates glycogen sunthase.
What would be the effects of a mammalian organism over expressing IRS-1 were also deficient in muscle GAK-3? Would this deficiency be lethal ?
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