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the small subunit binds tRNA and mRNA, the largesubunit forms peptide bonds
What is the primary role of galactose in metabolism and how is itaffected in galactosemia?
What are the possible reasons for the poor long-term outcome oftreated galactosemics?
Explain the extended elevation of blood fructose concentration inpatients with hereditary fructose intolerance (HFI).
Are fructose-1-phosphate aldolase and fructose-1,6-bisphosphatealdolase the same protein? In what pathway(s) does this enzymefunction?
Why didn’t GeorgeIII have relatives who exhibited a similar autosomal dominantdisorder?
How is lead poisoning related to heme biosynthesis? How would heavy metalsimpair heme biosynthesis?
What are three variables that determine the rate and extent of hemoglobinpolymer formation within erythrocytes?
How is sickle cell disease diagnosed clinically? What is the frequency of thedisease in different populations?
What are the general strategies to treat patients with sickle cell disease? Give anexample of each.
What is the mechanism by which STI571 (Gleevac) inhibits the Abl tyrosine kinase?
What type of enzyme inhibitor is STI571, and how would its mechanism of actionbe determined experimentally?
Describe the CK enzyme reaction. In what tissues does this reaction occur?
What isozymes are known for CK, and what is their tissuelocation?
What is the value of assaying for the CK MB isozyme in cardiology? How is theassay used?
What is the biochemical basis of Menkes disease, i.e. why mutations in the Menkesdisease gene (ATP7A) cause the disease?
Explain how normal Menkes disease (ATP7A) and Wilson’s disease (ATP7B) proteinswork and how they regulate copper metabolism. (see slide 352
What are the consequences of HER-2 over expression to intracellular signalingand to behavior of tumor cells?
Why would a medical oncologist be interested in whether or not a patient’s tumor overexpressed HER-2?
What is meant by a “humanized antibody”, and why are humanized antibodiessuch as trastuzumab effective as therapeutics?
Describe the biochemistry of Gaucher’s disease. Where does the affected enzymefunction on the histological and cellular level? inheritance?
Describe the genetics of Gaucher’s disease. Are mutations in the gene random or arethere specific mutations that predominate?
What clinical assessments are employed to identify patients who have Gaucher’sdisease?
How has enzyme replacement therapy (ERT) for Gaucher’s disease progressed overthe years and where does it stand today?
What is the downside of ERT therapy for Gauchers? What other therapy options are available andwhat are their downsides?
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