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Medical Sciences
Medical Sciences 4930F/G
Robert Gros

SIGNAL TRANSDUCTION PATHWAYS & ATHEROSCLEROSIS – Study Questions 1. What is signal transduction? What does it involve? 2. What are the 5 different signalling mechanisms? Which one is the most common drug target? 3. Why is endothelial dysfunction important for atherosclerosis development? How does it influence the growth of atherosclerosis at each step of development? 4. Why is inflammation important for the development of atherosclerosis? 5. What is hypertension a significant risk factor for? 6. Why do you likely have more than one risk factor if you have been confirmed with a risk factor? 7. What is the cycle associated with endothelial dysfunction and risk factors? 8. What are the hallmarks of atherosclerosis? What cells are involved? 9. What is the importance of endothelium in the maintenance of vascular health? 10. What signals are involved in the development of atherosclerosis? How? 11. Which cells are involved in regulating cardiac function? How do they help regulate? 12. What does dysregulation of these functions cause? 13. What is the receptor-G-protein-effector cascade? How is it important in atherosclerotic development? How does this pathway affect the cardiovascular system? 14. How does the receptor activate G-proteins? How do G-proteins activate effectors? 15. How are G-proteins deactivated? What deactivates them? 16. How do protein kinases affect the receptor-G-protein-effector cascade? 17. What are the different mechanisms used to regulate GPCRs? 18. What are the classical GPCRs? 19. What is a transducer? 20. What is the sequence of events regulating vascular smooth muscle contraction and relaxation? 21. Why are mutations of sphingosine-1 commonly associated with cardiovascular disease? 22. How do the agonists that mediate vasoconstriction differ from those that regulate vasodilation? Why are some involved in both pathways? 23. What is an example of where the same agonist is used to control both vasoconstriction and vasodilation but has a differe
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