This preview shows page 1. Sign up to view the full content.
Unformatted text preview: ntially providing an alternative to embryonic stem cells for transplantation therapy.
embryonic stem cell, pluripotency somatic cell nuclear transfer, therapeutic cloning, reproductive cloning induced pluripotent stem cell This material cannot be copied, reproduced, manufactured, or disseminated in any form without express written permission from the publisher. 2009 Sinauer Associates, Inc. UNCORRECTED PAGE PROOFS
CHAPTER 17 Questions
1. Why is cell death via apoptosis more advantageous to multicellular organisms than cell death via acute injury? 2. What molecular mechanisms regulate caspase activity? 3. You have expressed mutants of nuclear lamins in human fibroblasts. The Asp residue in the caspase cleavage site has been mutated to Glu in these lamins. How would these mutant lamins affect the progression of apoptosis? 4. How do Bcl-2 family proteins regulate apoptosis in mammalian cells? 5. How does p53 activation in response to DNA damage affect cell cycle progression and cell survival? 6. You have constructed a Bad mutant in which the Akt phosphorylation site has been mutated such that Akt no longer phosphorylates it. How would expression of this mutant affect cell survival? 7. How would expression of siRNA targeted against 14-3-3 proteins affect apoptosis? 8. You are considering treatment of a leukemic patient with TNF. Upon further analysis you determine that the leukemic cells have an inactivating mutation of caspase-8. Will treatment with TNF be an effective therapy for this patient? 9. How would siRNA against Ced-3 affect the development of C. elegans? 10. You have isolated a polypeptide from a toxic plant, which localizes to mitochondria after endocytosis by mammalian cells. The polypeptide aggregates and forms large channels in the mitochondrial outer membrane, releasing proteins from the intermembrane space into the cytoplasm. How will treatment with this polypeptide affect mammalian cells in culture? 11. Many adult tissues contain terminally differentiated cells that are incapable of proliferation. However, these tissues can regenerate following damage. What gives these tissues their regenerative capabilities? 12. What is the critical property of stem cells? 13. What are the potential advantages of embryonic stem cells as compared to adult stem cells for therapeutic applications? References and Further Reading
Programmed Cell Death
Danial, N. K. and S. J. Korsmeyer. 2004. Cell death: Critical control points. Cell 116: 205219. [R] Datta, S. R., A. Brunet and M. E. Greenberg. 1999. Cellular survival: A play in three Akts. Genes Dev. 13: 2902927. [R] Degterev, A. and J. Yuan. 2008. Expansion and evolution of cell death programmes. Nature Rev. Cell Mol. Biol. 9: 378390. [R] Ellis, H. M. and H. R. Horvitz. 1986. Genetic control of programmed cell death in the nematode C. elegans. Cell 44: 817829. [P] Hay, B. A. and M. Guo. 2006. Caspase-dependent cell death in Drosophila. Ann. Rev. Cell Dev. Biol. 22: 623650. [R] Hengartner, M. O. 2000. The biochemistry of apoptosis. Nature 407: 770776. [R] Holcik, M. and N. Sonenberg. 2005. Translational control in stress and apoptosis. Nature Rev. Mol. Cell Biol. 6: 318327. [R] Jacobson, M. D., M. Weil and M. C. Raff. 1997. Programmed cell death in animal development. Cell 88: 347354. [R] Jope, R. S. and G. V. W. Johnson. 2004. The glamour and gloom of glycogen synthase kinase-3. Trends Biochem. Sci. 29: 95102. [R] Lauber, K., S. G. Blumenthal, M. Waibel and S. Wesselborg. 2004. Clearance of apoptotic cells: Getting rid of the corpses. Mol. Cell 14: 277287. [R] Levine, B. and G. Kroemer. 2008. Autophagy in the pathogenesis of disease. Cell 132: 2742. [R] Riedl, S. J. and G. S. Salvesen. 2007. The apoptosome: signaling platform of cell death. Nature Rev. Mol. Cell Biol. 8: 405413. [R] Samejima, K. and W. C. Earnshaw. 2005. Trashing the genome: The role of nucleases during apoptosis. Nature Rev. Mol. Cell Biol. 6: 677688. [R] Spierings, D., G. McStay, M. Saleh, C. Bender, J. Chipuk, U. Maurer and D. R. Green. 2005. Connected to death: The (unexpurgated) mitochondrial pathway of apoptosis. Science 310: 6667. [R] Taylor, R. C., S. P. Cullen and S. J. Martin. 2008. Apoptosis: controlled demolition at the cellular level. Nature Rev. Mol. Cell Biol. 9: 231241. [R] Vaux, D. L. and J. Silke. 2005. IAPs, RINGs and ubiquitylation. Nature Rev. Mol. Cell Biol. 6: 287297. [R] Vousden, K. H. and X. Lu. 2002. Live or let die: The cells response to p53. Nature Rev. Cancer 2: 594604. [R] Wajant, H. 2002. The Fas signaling pathway: More than a paradigm. Science 296: 16351636. [R] Youle, R. J. and A. Strasser. 2008. The BCL-2 protein family: opposing activities that mediate cell death. Nature Rev. Mol. Cell Biol. 9: 4759. [R] Yu, J. and L. Zhang. 2005. The transcriptional targets of p53 in apoptosis control. Biochem. Biophys. Res. Comm. 331: 851858. [R] Zong, W.-X. and C. B. Thompson. 2006. Necrotic death as a cell fate. Genes Dev. 20: 115. [R] Stem Cells and the Maintenance of Adult Tissues
Barker, N., M. van de...
View Full Document