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Give examples and brief descriptions of pharmaceutical agents that work by altering responses in the RAS pathway.
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- List the three 'effector' signaling pathways activated by the Ras protein.Compare and contrast the regulation of Ras with trimeric G proteins.The Pathway presented shows you how the pathway is regulated with a Ras-GEF. Explain how adding a Ras-GAP to the cell would A) specifically affect the molecules of the signaling pathway and B) affect the response of the cell.
- Briefly describe the following properties of the Ras GTPases: a) Size, structure and cellular localization (for structure I want to know if they are lipidated and any other unique features) , b) How are they activated and inactivated (i.e. include the GEFs and GAPs), c). Give an example of downstream effector proteins, d). Are they or could they be involved in human cancer.Discuss the advantages and disadvantages of general chemotherapy like Etoposide compared to specific inhibition of EGFR.describe the outcome of EGFR inhibition as well as the differences between erlotinib and panitumumab’s mechanisms of action. EGFR- driven cancer cells can become resistant to tyrosine kinase inhibitors. Explain the two types of EGFR blockade acquired resistance and propose a subsequent treatment option.
- Describe the common signal transduction event that is perturbed by cancer-promoting mutations in the genes encoding RAS and NF-1. Why are mutations in RAS more commonly found in cancers than mutations in NF-1?A mutation in the Ras protein renders Ras constitutively active (RasD). What is constitutive activation?How does constitutively active Ras promote cancer?
- The egfr kinase independent transactivation of the ras pathway does require egfr. Explain this apparent contradiction.I come across a sentence "Myc mutations increase the lethality of Ras inhibitors", but am not sure if an increase in the lethality of Ras inhibitors is a good thing or bad thing. I should be grateful if the expert could help and advise.Even in the presence of a Ras-GAP, a single amino acid change in as renders it incapable of hydrolyzing GTP. This mutation is known as Ras+ and is a cancer-causing mutation. What effect do you think this mutation will have on signaling downstream of Ras+? Why? a)A mutation would turn on the signaling pathway all of the time. b)Even if a route is mutated, it can still be turned on or off. c)Due to a mutation, the signaling pathway would always be off.