Overview
Please answer the Questions according to the attached slides.
1. We described 2 oncogenes/proto-oncogenes that are each regulated at the level of protein stability (ie. protein is synthesized, but it is targeted for destruction). Name these 2 proteins. For each protein, describe what we learned about how the protein is regulated. Be as specific as possible, and provide at least 5 details/facts about the signaling pathway that leads to the protein’s stabilization.
2. If you were a normal cell interested in becoming transformed, what one gene would you mutate first to drive hyperproliferation? Choose a gene/protein we have already covered in class. But do NOT use either of the proteins from Q1 or P53 (we haven't learned enough about it yet). Do you know the "what 3 things would you take if you were stranded on a deserted island?" game? To start answering this question, list your "top" 3 choices for a gene to mutate in your quest to become a cancer. For full credit, provide the following:
List your 3 genes
What is the name of your top gene/protein?
What does your top protein normally do in the cell?
What would a mutation (associated with cancer) do to the function of the protein (activate or repress)?
Are both alleles required to be mutated or only one allele? Why?
Why is your top choice better than the other 2 for this first step in tumorigenesis?