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Please answer each question separately:
1. A few simple short answers just to make sure we are all on the same page.
A.Why might mutations in PTEN have different phenotypes from activating mutations in p110 alpha?
B.Comment on the statement “Growth factor activation of PI3K results from recruitment of the enzyme to the activated
receptor”.
C.How does the distribution of Class I and Class III enzymes and products in the cell compare?
D.What is the specificity of PH domains?
E.What is the relationship between AKT and mTORC (i.e. what do they do to each other?)?
2. E542K and E545K in the helical domain are hotspots for mutations in p110 alpha that are associated with cancer. What
hypotheses could you propose for why this might be so? (i.e. Why is the helical domain important?) What experiments would
you do to test those hypotheses. [There is some literature on this issue, but the intent here is not to look that up and cite it (it’s
incomplete in any case)].
3. PI3 kinase signaling is known to affect the levels of target proteins. Suppose you had such a protein that shows enhanced
expression when PI3K signaling is activated. What mechanisms (at least 4) could you propose to explain the results? What
experiments would you do to test each of the possibilities

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Posted on May 12, 2016Author TutorCategories Question, Questions