Using the AAV virus you created in the simulation, you introduce it to a mouse model for heart failure to determine the effect of SERCA2A in heart failure. a. Why would this virus only affect the myocardium and not other cell types within the mouse? b. Would the mouse then be able to spread that virus to other mice? Explain.

Which of the following drugs would you expect would prevent transformation of cells by the Rous Sarcoma Virus (RSV) (select all that appy)? A. Tyrosine Kinase Inhibitor B. Integrase Inhibitor C. Inhibitor GTPase Activity ✓ D. Reverse Transcriptase Inhibitor E. Staurosporine (inhibitor of Ser/Thr kinases)

You are studying a novel viral protein. There is nothing known about the function of this protein. You analyze the protein sequence you observe an N- terminal sequence that looks like a signal sequence. To determine whether this sequence is in fact a signal sequence you clone the gene and make a mutation in the sequence, changing all of the amino acids in that region to alanine. You then look to see if the protein binds SRP and is brought to the ER. If your hypothesis is correct and it is in fact a signal sequence you should get the following results to your experiment. Select the outcome that supports your hypothesis. WT = wild-type, unmutated protein M = mutant, protein with signal sequence mutated to alanines A. WT protein binds to SRP, localizes to ER M protein does not bind to SRP, is found in the cytosol B. WT protein does not bind SRP, localizes to the ER M protein does not bind to SRP, is found in cytosol C. WT protein does not bind to SRP, is found in the cytosol M protein…

What is an example where p27 kip1 can remain in the nucleus performing its inhibitory effect? A. When p27 kip1 mutant with Threonine to Alanine substitution is expressed. B. When a constitutively active Akt/PKB is expressed and interact with wild type p27 kip1 C. When a dominant-negative Akt/PKB is expressed D. A and C are correct.