The brain is fueled almost exclusively by glucose. Using this fact, would it be a good idea to express glucose-1-phosphatase in muscle? What type of phenotype would be exhibited by a mouse expressing glucose-1-phosphatase in muscle?

What is meant by intrinsic GTPase activity? Exchange of GDP for GTP on the a-subunit of the G protein Inhibition of GBCR receptor activity Activation of Adenylyl Cyclades Breakdown of cAMP by phosphodiesterase Spontaneous hydrolysis of GTP on the a-subunit of the G-protein

Normally, when blood glucose level increases (e.g. after a meal), the islet cells in the pancreas secrete insulin. When insulin molecules bind to insulin receptors on the surface of a muscle cell, the receptors become activated, initiating a signaling pathway which eventually results in the increase in the number of passive glucose transporter on the muscle cell surface thus increases the uptake of glucose into the cell and decrease blood glucose level. Indicate whether the following conditions/practice will likely lead to diabetes (mark Yes or No). [Select] degeneration of islet cells [Select] [Select] [Select] a mutation in the insulin receptor that increases its kinase activity ✓ exercise a mutation in the insulin receptor that prevents dimerization

You decide to investigate cell signaling of a pair of newly identified GPCRs, GPCR-W and GPCR-Z. Each binds the same ligand, but activates different downstream heterotrimeric G-proteins that act on adenylyl cyclase. You discover that ligand binding has opposite effects on adenylyl cyclase activity for each receptor. GPCR-W causes an increase in adenylyl cyclase activity, while GPCR-Z causes a decrease in adenylyl cyclase activity. You obtain a cell line expressing GPCR-W, GPCR-Z, the relevant G-proteins, and adenylyl cyclase. There is baseline adenylyl cyclase activity producing a baseline amount of cAMP. You embark on a research project to characterize the following mutations in the components of the signaling pathway. 2. Will each of the following mutations increase or decrease the levels of cAMP inside the cell upon adding the ligand to the cell culture? A mutation in Gi that prevents release of bound GDP. A mutation in Gs that prevents GTP hydrolysis. A mutation in Gi that…

Steroid hormones are required by the body at puberty and into adolescence to regulate growth and cell division at more rapid pace than in later life.  This regulation occurs via their interaction with cellular receptors and the signaling cascades/pathways that follow.  Describe for me the difference between the two major classes of steroids, anabolic and catabolic steroids.  What might you expect the result of signaling cascades to be in cells receiving either anabolic or catabolic “signals”? (B) At some point in late adolescence, steroid production decreases by almost 100 fold, as we transition into “adulthood”.  Why might we wish to stop these signals from constantly being in our blood stream, (like, Say, between 17-24 years of age)?  What result might these steroids have on cancer cells where abhorrent signaling is already causing an increased rate of cell division/growth? Could steroid use result in Cancer?

A fixed amount of radiolabelled insulin was incubated with a fixed amount of anti-insulin antibody, the bound ligand was separated from free ligand at different time intervals. Draw a diagram of the concentration of the insulin/antibody complex with time. (Insulin/antibody complex is the bound ligand) asap typed only .

Epinephrine stimulates glycogen breakdown by activating glycogen phosphorylase. However, in the research lab, no glycogen breakdown occurred when epinephrine was added to a test tube containing the enzyme and its substrate, glycogen. Explain why glycogen phosphorylase could be activated by epinephrine only when the hormone was added to intact cells in a solution.

Which of the following steps amplify the epinephrine signal response in cells: receptor activation of G protein, G protein activation of adenylyl cyclase, cAMP activation of PKA, or PKA phosphorylation of glycogen phosphorylase kinase (GPK)? Which change will have a greater effect on signal amplification: an increase in the number of epinephrine receptors or an increase in the number of Gαs  proteins?

Which of the following best describes the use of 2-deoxyglucose in allowing for cancer therapy? Elevates p53 levels directly to regulate glycolytic flux Blocks activation of HIF1transcriptional activation Diminishes lactate production by inhibiting lactate dehydrogenase to allow increased levels of pyruvate to force the transport of pyruvate into the matrix and the function of the TCA cycle Diminishes lactate export from the cell to allow increased levels of pyruvate to force the transport of pyruvate into the matrix and the function of the TCA cycle Competes with glucose for hexokinase, allowing inhibition of glycolytic flux, reducing ATP production.

You decide to investigate cell signaling of a pair of newly identified GPCRs, GPCR-W and GPCR-Z. Each binds the same ligand, but activates different downstream heterotrimeric G-proteins that act on adenylyl cyclase. You discover that ligand binding has opposite effects on adenylyl cyclase activity for each receptor. GPCR-W causes an increase in adenylyl cyclase activity, while GPCR-Z causes a decrease in adenylyl cyclase activity. You obtain a cell line expressing GPCR-W, GPCR-Z, the relevant G-proteins, and adenylyl cyclase. There is baseline adenylyl cyclase activity producing a baseline amount of cAMP. You embark on a research project to characterize the following mutations in the components of the signaling pathway. 2. Will each of the following mutations increase or decrease the levels of cAMP inside the cell upon adding the ligand to the cell culture? A mutation in GPCR-W that prevents G-protein activation? A mutation in GPCR-Z that prevents G-protein activation? A mutation in…