Name two proteins that are effectors of the insulin signaling pathway in adipocytes, liver, or muscle cells. Explain how these effector proteins address the conditions that triggered insulin release
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Name two proteins that are effectors of the insulin signaling pathway in adipocytes, liver, or muscle cells. Explain how these effector proteins address the conditions that triggered insulin release.
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- 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 PKBPKBof but not the activation of PKPK.Describe two features of insulin signaling that affect glucose utilization. Aβ-adrenergic response can be modulated through the actions of a receptorkinase and arrestin because phosphorylation by the kinase desensitizes thereceptor. How might signaling by a tyrosine receptor kinase, such as theinsulin receptor, be modulated?In some forms of diabetes, a mutation in the b subunit of the insulin receptor abolishes the enzymatic activity of that subunit. How does the mutation affect the cell’s response to insulin? Can additional insulin (e.g., from injections) overcome the defect?
- In a hypothetical cAMP-mediated signal transduction cascade, the GTP-αs/adenylate cyclase interaction following a single hormone–receptor binding event lasts for 2.3 seconds. The catalytic rate (turnover number) for the adenylate cyclase in question is 350 cAMP molecules produced per second. How many cAMP molecules would be produced if five hormone-receptor binding events were to occur before the hormone molecule dissipates in the bloodstream? What is the amplification effect of this step in the signaling pathway?Please identify the incorrect statement about hormone signaling: A) Cystolic receptors bind to hydophobic hormones and transport them into the nucleus where they directly influence protein synthesis. B) Hydropholic hormones cannot pass through the plasma membrane without help. Therefore, there are transport proteins that carry the hydrophillic hormones to the cytosol where it can bind its receptor C) Hydrophilic hormone signalling involves membrane receptors that have the ability to activate adenylyl cyclase, producing cAMP. cAMP then affects the activity of numerous proteins in the cytoplam. D) Hydrophobic hormones easily enter the plasma membrane. Therefore, there is no need for hydrophinic hormone receptors to be on the extracellular surface.What is the ligand(signaling molecule) in a(an) insulin signaling pathway and what causes this ligand to be sent out?
- The physiological effects of epinephrine should in principle be mimicked by addition of cAMP to the target cells. In practice, addition of cAMP to intact target cells elicits only a minimal physiological response. Why? When the structurally related derivative dibutyryl cAMP (shown below) is added to intact cells, the expected physiological response is readily apparent. Explain the basis for the difference in cellular response to these two substances. Dibutyryl cAMP is widely used in studies of cAMP function.HbA1c is used to monitor blood glucose levels because hemoglobin is the only protein in blood that is covalently modified by glucose. True False Insulin Glargine is a long-acting form of insulin that is synthesized with several D-amino acids that slow its proteolytic degradation and extend the half-life of the insulin Glargine molecule. True FalseCompare the localization of GLUT4 with that of GLUT2 and GLUT3, and explain why these localizations are important in the response of muscle,adipose tissue, brain, and liver to insulin
- What are the steps involved in synthesis of genetically engineered insulin.Mutations in glucokinase which lower the kcat for the enzyme or elevate the Km for glucose result in mild to moderate elevation of blood glucose. Explain how these mutations cause diabetes-like symptoms in patients.Based on your understanding of the binding of insulin, select all of the following events that you would expect to occur in muscle cells due to insulin binding to receptors.Group of answer choices a. Glycogen synthesis is activated b. PFK is stabilized in the R-state and glycolysis is activated c. GLUT4 (transporters) are increased in concentration at the plasma membrane d. Fructose 2,6-bisphosphate increased levels aid in stabilization of the T-state fructose 1,6-bisphosphatase e. Gluconeogenesis is activated in response to elevated fructose 2,6-bisphosphate levels f. Phosphorylation cascades allow for covalent modifications that would aid in the breakdown of glycogen to allow for increased levels of glucose 6-phosphate in the cell g. Hexokinase is inhibited so glucose will not be brought into the cell in high amounts h. Glycogen breakdown pathway is inactivated