Study Question Sets for Exam 3
Study Question Set 15 - Cell Signaling - 2
Enzyme-linked Receptors

1. Discuss the importance of the GTPase activities of G-proteins and other GTP binding proteins in cell signaling pathways.
2. Indicate the initial events whereby phosphorylation of tyrosine residues on a protein results in "downstream events" in a signaling pathway.
3. Since ligand binding to Receptor Tyrosine Kinases inhibits GAP activity, what is the general effect of ligand binding to these receptors on RTK signalling pathways?
4. What reactions are catalyzed by phosphatidyl inositol 3 phosphate kinase?
5. Explain the importance of PI3 Kinase and phosphatidyl 3,4,5 trisphosphate to recruiting signaling molecules to the plasma membrane.
6. Describe the chain of events whereby binding of PDGF to its receptor results in activation of ras.
7. Explain the relationship between sos and ras in the PDGF signaling pathway.
8. Explain briefly the effects of inhibiting the GAP for ras (for example, by its binding to phosphotyrosines of PDGFR) on the activities of ras signaling pathways.
9. What is a "MAPK"?
10. What is the origin of the name "MAP kinase"? Explain.
11. Describe the chain of events whereby binding of platelet derived growth factor (PDGF) to its receptor results in activation of gene expression. Is this the only type of response to binding of PDGF to its receptor? Explain.
12. What would happen if a cell contained a mutant Ras protein that was in a permanently "on" state?
13. What is apoptosis? Why would apoptosis be useful to an organism when a cell has damaged DNA that is not repaired?
14. Why would deleterious mutations in both of a cell's genes for p53 be a major contributor to cancer?
15. How is it that a single type of extracellular signaling ligand binding a 7-pass receptor can alter a variety of enzyme activities in a single cell?
16. Is it possible that a single type of extracellular signaling ligand binding a 7-pass receptor can alter the behavior of more than one type of effector?   Explain.
17. How is it that a single extracellular signaling ligand for a receptor tyrosine kinanse can alter more than one signaling pathway? (Hint: Consider phosphorylations on multiple tyrosines.)
18. Are cell signaling pathways involving heterotrimeric G proteins completely independent of pathways involving receptor tyrosine kinases? Explain, giving at least one example.
19. Explain the most obvious difference between Receptor Tryosine Kinases and Tryosine Kinase Associated Receptors in terms of how tyrosine phosphorylation is activated.
20. Explain the basis for the acronym STAT.
21. Describe the general steps involved in alteration of gene transcription in response to receptor binding of a cytokine such as alpha interferon.
22. Describe the general steps involved in alteration of gene expression in response to binding of transforming growth factor - beta (TGF-beta) to its receptor.
23. Identify (and compare where appropriate) the following:
1. histidine protein kinase
2. receptor guanylyl cyclase
3. receptor tryosine kinase, tryosine kinase-coupled receptor, non-receptor tyrosine kinase
4. MAP kinase, MAP kinase kinase, MAP kinase cascade, raf, MEK, ERK
5. SRE (Serum Response Element), SRF (Serum Response Factor)
6. pp90^rsk
7. src, SH2 domain, SH3 domain
8. PH domain, PI(3,4,5,)P₃
9. PTB domain
10. monomeric GTPase
11. mitogen
12. GEF, GAP
13. p53
14. grb 2
15. sos
16. Jak
17. Tyk-2
18. STAT
19. Smad

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