Name: Student IID BC403-001/230 Problem Set #2 Due: 2/28/2018 15 points Instruct

Question

Name: Student IID BC403-001/230 Problem Set #2 Due: 2/28/2018 15 points Instructions: Please answer the following questions as fully as you can while being concise with your answer. You may work together and use any and all resources available to you. Each student is expected to hand-in their own work and plagiarism is unacceptable and will result in a zero for the assignment. Multiple offenses will be met with more severe consequences. For problems that require mathematical calculation your work must be shown to receive full credit. 1. Research in cell biology and metabolism has progressed due to the discovery of molecules that artificially stimulate or inhibit glucagon/epinephrine and insulin signaling pathways. Let's say you are working in a lab cataloging the effects of a library of small molecules on these pathways and have a "hi" on molecule 1stAVNGR. Preliminary data on molecule 1stAVNGR indicates that the cardiac isoform of PFK2/FBPase2 is doubly phosphorylated when this molecule is present at micromolar concentrations in cell cultures. Given this context answer the following questions. Under these conditions what is the predicted degree of association between the regulatory subunits and the catalytic subunits of PKA? (1 point) a. Further investigation of molecule 1stAVNGR indicates elevated levels of cAMP within the cell despite the absence of epinephrine or glucagon. Hypothesize two possible explanations for this data. (4 points) b. When cell cultures are given both molecule 1stAVNGR and molecule RedSKLL (a G-protein inhibitor) CAMP levels remain high (again despite the absence of epinephrine or glucagon). Given this new information hypothesize a possible explanation for the data(2 points) c.

Explanation / Answer

For this exercise it is necessary to know that PFK is an enzyme that catalyzes the conversion of fructose 6 phosphate to fructose 1,6-bisphosphate. Additionally this enzyme is the most important cotrol element of glycolysis in mammals. This enzyme is inhibited in an allosteric way by high noles of ATP (that is to say that the cell has a good energetic level): ATP binds to the enzyme and with this diminishes the affinity for its substrate (with this it makes a sigmoid graph). While the AMP (cell with low energetic level) counteracts the inhibitory activity of ATP.

For the part a)

Now, since we know how this enzyme works (which by the way is a tetrameric enzyme): The molecule 1stAVNGR can function as an analogue of the AMP, because if there is more phosphorylation it is because the cell feels that it has low energectic levels. The molecule must increase its affinity for the substrate (fuctose 6 phosphate) to convert it to fructose 1,6-bisphosphate. That is to say the molecule 1stAVNGR when joining the regulatory subunits of the active enzyme to the catalytic subunits for the reaction to take place.

For the part b)

For this we must remember that adrenaline (epinephrine) and glucagon are hormones that stimulate glycogenolysis through the membrane proteins known as adenylate cyclase which convert ATP into cAMP directly to indicate to the cell a low energetic level. This is related to the fleeing or fighting response (an evolutionary mechanism). One possible explanation is that the 1stAVNGR molecule works like glucagon or adrenaline joining the receptor (adenylate cyclase) to generate cAMP.

Since we do not know the nature of the 1stAVNGR molecule, if it is non-polar, it can cross the cell membrane and bind to other cAMP-generating enzymes, one of which is adenylate kinase which, from two molecules of ADP, generates an ATP molecule. an AMP molecule.

For the part c)

remember that G proteins are membrane proteins which are mediated by GTP and these can inhibit or stimulate adenylate cyclase, which would reinforce the previous theory I proposed which says that 1stAVNGR is a non-polar molecule that crosses the membrane and activates other proteins that generate AMP (as adenylate kinase would be)

For the part d)

In this case, 1stAVNGR is an enzyme that favors the flow of glycolysis, although there is enough ATP (an adequate energy level) it produces effects in which cAMP is formed. Given that cAMP is a regulator of the PFK enzyme, it will generate this enzyme to remain activated (that is, its affinity for the substrate will remain high) with which the fructose 6 phosphate will be phosphorylated to fructose 1,6 bisphosphate. the glycolysis path will follow normally.

For part e)

In the liver, the regulation of glulisis is somewhat different because in this case the PFK is regulated by other molecules. Regarding the ATP, the regulation is the same. However, the agents that inhibit it find citrate (a finger that the liver is a vice in which many precursors are synthesized and it is a meteorological pool of them).
In this case, 1stAVNGR would estimate the glycolytic flow of the route because having high levels of cAMP the cell will feel that it has low levels of energy for which the glycolytic route will be stimulated. However, we do not know how much it would take an additional experiment comparing the activity of the route against fructose 2,6 bisphosphate, which is a potent activator of glycolysis in liver. Which activates even more the PFK and for that reason it is necessary to compare the effect of the way against this other stimulator (which by the way is how the liver responds to the high levels of glucose in blood)

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