Problem%20Set_4 - 1) Myc is an oncogenic transcription...

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1) Myc is an oncogenic transcription factor that regulates cell growth and division. When myc is overexpressed in cells they are transformed (i.e. they grow uncontrollably). During a cloning experiment you unexpectedly fused myc to the estrogen receptor (ER). When the myc-ER fusion is introduced into cells you see the following results: Construct Estrogen Cell Growth 1) myc None Yes 2) myc Yes Yes 3) ER None No 4) ER Yes No 5) myc-ER None No 6) myc-ER Yes Yes A) Why does fusion of myc to ER create an estrogen responsive oncogene? B) You fuse myc to a mutant estrogen receptor that no longer binds hsp90. Does this fusion cause transformation? Is it estrogen responsive? Briefly explain your reasoning. 2)You are watching the Super Bowl and you see 20 advertisements for Viagra. Each one ends with the following warning "Do not use if you are taking nitrates to treat angina since it might cause a catastrophic drop in blood pressure." A) Diagram the pathway that nitrates, such as nitroglycerine, use to treat angina. B) Using the diagram in A, explain where Viagra acts in the Nitric Oxide signaling pathway. C) Why does combining Viagra together with nitrates cause a catastrophic drop in blood pressure?
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3) You’re studying cellular signaling through G-Protein Coupled Receptors (GPCRs). Specifically you’re working on a pair of newly identified GPCRs, GPCR-A and GPCR- B. Each binds the same small ligand, but activates different heterotrimeric G-proteins that act on adenylyl cyclase. A) Your grad student mentor explains that both the receptors and the G α and G βγ subunits of the heterotrimeric G-proteins are membrane associated. You’re puzzled, because although you find obvious transmembrane domains in the receptor, you find none in G α and G βγ . How are G α and G βγ associated with the membrane (be specific)? B)
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This note was uploaded on 05/26/2010 for the course BICD BICD 110 taught by Professor Zao during the Winter '09 term at UCSD.

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Problem%20Set_4 - 1) Myc is an oncogenic transcription...

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