Glycogen is a complex polymer of glucose molecules involved in the storage of energy in many organisms. Depending on the signals received by a cell, different enzymes are activated, which will lead to either the synthesis or breakdown of glycogen. The product of glycogen breakdown, glucose 1-1-phosphate, can be modified into glucose 0-0-phosphate, an intermediate of glycolysis (Figure 1). Glycogen Glucose 0- Phosphate Gyooom Glycopen Figure 1. Glycogen synthesis and breakdown In the liver, glycogen synthase and glycogen phosphorylase are regulated by kinases. These kinases transfer phosphate groups from ATPATP to amino acids in glycogen synthase and glycogen phosphorylase. Phosphorylase kinase BB (PKB) is a kinase that regulates glycogen synthase kinase 33(GSK3) activity. GSK3 regulates the activity of glycogen synthase. Phosphorylase kinase (PKPK) regulates the activity of glycogen phosphorylase. The activity of these kinases depends on the activation of signaling pathways in response to the binding of specific cell signals, including insulin and glucagon, to their receptors (Figure 2). Cal Union Figure 2. A simplified model of signaling pathways in a liver cell that are activated by insulin and glucagon (a) A cell where PKBPKB is always active has a mutation that results in the permanent activation of GSKOGSK.3. Based on the information in Figure 2, predict the effect of this mutation on the activity of glycogen synthase. Justify your prediction. (b) (b) Describe the process that results in the activation of multiple copies of PKBPKB in response to the binding of a single molecule of insulin to its receptor. Explain why insulin can stimulate the activation PKBPKB of but not the activation of PKPK. (c) (c) Explain why an increase in glycogen phosphorylase activity might result in an increase in Q2 consumption in the cell. (d) (d) A certain type of tumor results in the overproduction of glucagon. Researchers claim that treatment with insulin can counteract the effects of the excess glucagon on the pathway shown in Figure 2. Provide reasoning to justify the researchers' claim