Study Question Sets for Exam 3
Study Question Set 14 -- Cell Signaling - 1
Heterotrimeric G Proteins, cAMP, and Calcium

  1. What types of signaling molecules have receptors that are in the cytoplasm or the nucleus of their target cells? How do such signaling molecules cause changes in cell activities?
  2. What types of signaling molecules typically use cell surface receptors to initiate response events in cells?
  3. NO (nitric oxide) does not have a specific cellular receptor. How, then, does it act as a signlaing molecule?
  4. Describe the structure of heterotrimeric G-proteins. How are these G-proteins associated with the membrane?
  5. Describe the typical structure of a heterotrimeric G-protein-linked receptor.
  6. Explain how it is that a 7-pass receptor bound by its extracelular signaling ligand acts as a GEF for a heterotrimeric G protein.
  7. Describe the "GTPase cycle" of a G-protein. nbsp; Relate this cyce to the sequence of events whereby the binding of a ligand to its seven-pass receptor is communicated into a modification in the behavior of a relevant effector (such as a ligand-gated channel or an enzyme).
  8. Explain the importance of the GTPase activity of the alpha-subunits of heterotrimeric G proteins to the termination of a signaling event.   What happens if the extracellular signaling molecule continues ot bind to the 7-pass receptor?
  9. Distinguish among Gs, Gi, and Go in terms of their effects on adenylyl cyclase.   Give other examples of opposing effects caused by activating different heterotrimeeric G proteins.
  10. Explain how it is possible that two different singlaling molecules binding to their respective seven-pass receptors can bring about similar responses within a cell.   (Hint: Is there a separate type of G-protein for each molecular response?)
  11. Explain how activation of one type of heterotrimeric G protein might lead to activation or inhibition of more than one type of effector.  Be thorough.
  12. Describe in general terms the role of protein kinases in cellular signaling.
  13. Indicate two ways in which phosphorylation of proteins on specific serines or threonines by protein kinases could lead to a cellular response.
  14. What is the role of serine/threonine phosphoprotein phosphatases in cell signal transduction? Why is this important?
  15. Most phosphoprotein phosphatases in eukaryotic cells are constitutively active. nbsp; Why is this important to the overall process of cell signaling?
  16. How does cAMP activate protein kinase A (PKA)?
  17. Explain the role of cAMP phosphodiesterase in limiting or terminating the activation of PKA by cAMP?
  18. What are "A Kinase Anchoring Proteins"?   What is their significance to localized cellular responses to elevated levels of cAMP?
  19. Explain how activation of a few molecules of PKA can lead to rapid elevation of the activities of several metabolic enzymes.
  20. Explain how activation of a few molecules of PKA can lead very quickly to production of huge numbers of products by PKA-activated enzymes.
  21. How can elevated concentrations of cAMP activate gene expression in eukaryotes?
  22. Explain why the effects of gene activation by activated PKA develop more slowly and last for a much longer time than activation of metabolic enzymes by PKA.
  23. Cyclic AMP and calcium are two major intracellular messenger molecules.  Elevated [cAMP] and elevated [Ca+2] give produce the same effects on the activities of some enzymes, yet they can give rise ot opposite responses of other enzymes. How is this possible? (Your answer should consider the diversity in protein kinases.)
  24. Using effects on adenylyl cyclase as a focus, explain how multiple positive and negative signaling pathways can "sum" to give graded cellular responses.   Include examples in your response.
  25. Does the beta-gamma component of a G protein have any role other than binding to the alpha subunit? Explain briefly.
  26. How does the GTPase activity of the alpha subunits of heterotrimeric G proteins affect signaling mediated by beta-gammma complexes?   Explain.
  27. Explain how receptors activating Gq can provide two types of signaling molecules.
  28. What is the major source of Ca+2 for the rapid increase of cytosolic [Ca2+] in responses occurring in epithelial cells?
  29. What is the major source of increased cytosolic [Ca+2] for activating CaM Kinase II in brain cells?
  30. What is the evolutionary significance of calmodulin?
  31. Explain the role of calmodulin in mediating many of the effects of elevated [Ca+2] in cells.   Your answer should include information about the stoichiometry of calcium binding and about the effects of that calcium binding on CaM behavior as it relates to cell signaling.
  32. Explain how elevated calcium levels activate CaM Kinase II.
  33. Explain how CaM Kinase II is able to have "molecular memory".
  34. Identify and compare the following:   protein kinase A (PKA), PKC, PKG, phosphorylase kinase.
    35.
  35. Identify the following:
    36.
    1. cAMP, cGMP, diacylglycerol, PI(4,5)P2, IP3, phospholipase C
    2. effector
    3. ligand-gated channel
    4. Gs, Gi, Go, Gq

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Last updated 3/23/2006
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