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Cell Growth and Development

Partial Cleavage of RasGAP by Caspases Is Required for Cell Survival in Mild Stress Conditions

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Pages 10425-10436 | Received 03 Apr 2004, Accepted 03 Sep 2004, Published online: 27 Mar 2023

REFERENCES

  • Alam, A., Cohen L. Y., Aouad S., and Sekaly R. P.. 1999. Early activation of caspases during T lymphocyte stimulation results in selective substrate cleavage in nonapoptotic cells. J. Exp. Med. 190:1879–1890.
  • Algeciras-Schimnich, A., Barnhart B. C., and Peter M. E.. 2002. Apoptosis-independent functions of killer caspases. Curr. Opin. Cell Biol. 14:721–726.
  • Baker, M. S., Chen X., Cao X. C., and Kaufman D. B.. 2001. Expression of a dominant negative inhibitor of NF-κB protects MIN6 beta-cells from cytokine-induced apoptosis. J. Surg. Res. 97:117–122.
  • Brazil, D. P., Park J., and Hemmings B. A.. 2002. PKB binding proteins. Getting in on the Akt. Cell 111:293–303.
  • Budihardjo, I., Oliver H., Lutter M., Luo X., and Wang X.. 1999. Biochemical pathways of caspase activation during apoptosis. Annu. Rev. Cell Dev. Biol. 15:269–290.
  • Campbell, D. S., and Holt C. E.. 2003. Apoptotic pathway and MAPKs differentially regulate chemotropic responses of retinal growth cones. Neuron 37:939–952.
  • Cauwels, A., Janssen B., Waeytens A., Cuvelier C., and Brouckaert P.. 2003. Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phospholipase A2. Nat. Immunol. 4:387–393.
  • Chun, H. J., Zheng L., Ahmad M., Wang J., Speirs C. K., Siegel R. M., Dale J. K., Puck J., Davis J., Hall C. G., Skoda-Smith S., Atkinson T. P., Straus S. E., and Lenardo M. J.. 2002. Pleiotropic defects in lymphocyte activation caused by caspase 8 mutations lead to human immunodeficiency. Nature 419:395–399.
  • De Botton, S., Sabri S., Daugas E., Zermati Y., Guidotti J. E., Hermine O., Kroemer G., Vainchenker W., and Debili N.. 2002. Platelet formation is the consequence of caspase activation within megakaryocytes. Blood 100:1310–1317.
  • De Maria, R., Zeuner A., Eramo A., Domenichelli C., Bonci D., Grignani F., Srinivasula S. M., Alnemri E. S., Testa U., and Peschle C.. 1999. Negative regulation of erythropoiesis by caspase mediated cleavage of GATA-1. Nature 401:489–493.
  • Deveraux, Q. L., and Reed T. C.. 1999. IAP family proteins—suppressors of apoptosis. Genes Dev. 13:239–252.
  • Dull, T., Zufferey R., Kelly M., Mandel R. J., Nguyen M., Trono D., and Naldini L.. 1998. A third-generation lentivirus vector with a conditional packaging system. J. Virol. 72:8463–8471.
  • Dupraz, P., Rinsch C., Pralong W. F., Rolland E., Zufferey R., Trono D., and Thorens B.. 1999. Lentivirus-mediated Bcl-2 expression in βTC-tet cells improves resistance to hypoxia and cytokine-induced apoptosis while preserving in vitro and in vivo control of insulin secretion. Gene Ther. 6:1160–1169.
  • Enari, M., Sakahira H., Yokoyama H., Okawa K., Iwamatsu A., and Nagata S.. 1998. A caspase activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD. Nature 391:43–50.
  • Fernando, P., Kelly J. F., Balazsi K., Slack R. S., and Megeney L. A.. 2002. Caspase 3 activity is required for skeletal muscle differentiation. Proc. Natl. Acad. Sci. USA 99:11025–11030.
  • Fischer, U., Janicke R. U., and Schulze-Osthoff K.. 2003. Many cuts to ruin: a comprehensive update of caspase substrates. Cell Death Differ. 10:76–100.
  • Giannoukakis, N., Rudert W. A., Trucco M., and Robbins P. D.. 2000. Protection of human islets from the effects of interleukin-1β by adenoviral gene transfer of an IκB repressor. J. Biol. Chem. 275:36509–36513.
  • Henkemeyer, M., Rossi D. J., Holmyard D. P., Puri M. C., Mbamalu G., Harpal K., Shih T. S., Jacks T., and Pawson T.. 1995. Vascular system defects and neuronal apoptosis in mice lacking Ras GTPase activating protein. Nature 377:695–701.
  • Holler, N., Tardivel A., Kovacsovics-Bankowski M., Hertig S., Gaide O., Martinon F., Tinel A., Deperthes D., Calderara S., Schulthess T., Engel J., Schneider P., and Tschopp J.. 2003. Two adjacent trimeric Fas ligands are required for Fas signaling and formation of a death-inducing signaling complex. Mol. Cell. Biol. 23:1428–1440.
  • Irmler, M., Thome M., Hahne M., Schneider P., Hofmann K., Steiner V., Bodmer J.-L., Schröter M., Burns K., Mattmann C., Rimoldi D., French L. E., and Tschopp J.. 1997. Inhibition of death receptor signals by cellular FLIP. Nature 388:190–195.
  • Jaeschke, H., Farhood A., Cai S. X., Tseng B. Y., and Bajt M. L.. 2000. Protection against TNF-induced liver parenchymal cell apoptosis during endotoxemia by a novel caspase inhibitor in mice. Toxicol. Appl. Pharmacol. 169:77–83.
  • Jarpe, M. B., Widmann C., Knall C., Schlesinger T. K., Gibson S., Yujiri T., Fanger G. R., Gelfand E. G., and Johnson G. L.. 1998. Anti-apoptotic versus pro-apoptotic signal transduction: checkpoints and stop signs along the road to death. Oncogene 17:1475–1482.
  • Jordan, M., Schallhorn A., and Wurm F. M.. 1996. Transfecting mammalian cells: optimization of critical parameters affecting calcium-phosphate precipitate formation. Nucleic Acids Res. 24:596–601.
  • Kataoka, T., Budd R. C., Holler N., Thome M., Martinon F., Irmler M., Burns K., Hahne M., Kennedy N., Kovacsovics M., and Tschopp J.. 2000. The caspase 8 inhibitor FLIP promotes activation of NF-κB and Erk signaling pathways. Curr. Biol. 10:640–648.
  • Kennedy, N. J., Kataoka T., Tschopp J., and Budd R. C.. 1999. Caspase activation is required for T cell proliferation. J. Exp. Med. 190:1891–1896.
  • Kulkarni, S. V., Gish G., Van der Geer P., Henkemeyer M., and Pawson T.. 2000. Role of p120 ras-GAP in directed cell movement. J. Cell Biol. 149:457–470.
  • Lakhani, S., and Flavell R. A.. 2003. Caspases and T lymphocytes: a flip of the coin? Immunol. Rev. 193:22–30.
  • Liston, P., Fong W. G., and Korneluk R. G.. 2003. The inhibitors of apoptosis: there is more to life than Bcl2. Oncogene 22:8568–8580.
  • McLaughlin, B., Hartnett K. A., Erhardt J. A., Legos J. J., White R. F., Barone F. C., and Aizenman E.. 2003. Caspase 3 activation is essential for neuroprotection in preconditioning. Proc. Natl. Acad. Sci. USA 100:715–720.
  • Newton, K., and Strasser A.. 2003. Caspases signal not only apoptosis but also antigen-induced activation in cells of the immune system. Genes Dev. 17:819–825.
  • Nicholson, D. W., and Thornberry N. A.. 1997. Caspases: killer proteases. Trends Biochem. Sci. 22:299–306.
  • Reed, J. C. 1998. Bcl-2 family proteins. Oncogene 17:3225–3236.
  • Ryan, K. M., Ernst M. K., Rice N. R., and Vousden K. H.. 2000. Role of NF-κB in p53-mediated programmed cell death. Nature 404:892–897.
  • Sakahira, H., Enari M., and Nagata S.. 1998. Cleavage of CAD inhibitor in CAD activation and DNA degradation during apoptosis. Nature 391:96–99.
  • Salmena, L., Lemmers B., Hakem A., Matysiak-Zablocki E., Murakami K., Au P. Y., Berry D. M., Tamblyn L., Shehabeldin A., Migon E., Wakeham A., Bouchard D., Yeh W. C., McGlade J. C., Ohashi P. S., and Hakem R.. 2003. Essential role for caspase 8 in T-cell homeostasis and T-cell-mediated immunity. Genes Dev. 17:883–895.
  • Schlesinger, T. K., Bonvin C., Jarpe M. B., Fanger G. R., Cardinaux J.-R., Johnson G. L., and Widmann C.. 2002. Apoptosis stimulated by the 91-kDa caspase cleavage MEKK1 fragment requires translocation to soluble cellular compartments. J. Biol. Chem. 277:10283–10291.
  • Shi, Y. 2002. Mechanisms of caspase activation and inhibition during apoptosis. Mol. Cell 9:459–470.
  • Slee, E. A., Harte M. T., Kluck R. M., Wolf B. B., Casiano C. A., Newmeyer D. D., Wang H. G., Reed J. C., Nicholson D. W., Alnemri E. S., Green D. R., and Martin S. J.. 1999. Ordering the cytochrome c-initiated caspase cascade: hierarchical activation of caspases-2, -3, -6, -7, -8, and -10 in a caspase 9-dependent manner. J. Cell Biol. 144:281–292.
  • Stroh, C., and Schulze-Osthoff K.. 1998. Death by a thousand cuts: an ever increasing list of caspase substrates. Cell Death Differ. 5:997–1000.
  • Thornberry, N., and Lazebnik Y. A.. 1998. Caspases: enemies within. Science 281:1312–1316.
  • Utz, P. J., and Anderson P.. 2000. Life and death decisions: regulation of apoptosis by proteolysis of signaling molecules. Cell Death Differ. 7:589–602.
  • Valius, M., Secrist J., and Kazlauskas A.. 1995. The GTPase activating protein of ras suppresses platelet-derived growth factor β receptor signaling by silencing phospholipase c-γ1. Mol. Cell. Biol. 15:3058–3071.
  • Van der Geer, P., Henkemeyer M., Jacks T., and Pawson T.. 1997. Aberrant Ras regulation and reduced p190 tyrosine phosphorylation in cells lacking p120-Gap. Mol. Cell. Biol. 17:1840–1847.
  • Vercammen, D., Beyaert R., Denecker G., Goossens V., Van Loo G., Declercq W., Grooten J., Fiers W., and Vandenabeele P.. 1998. Inhibition of caspases increases the sensitivity of L929 cells to necrosis mediated by tumor necrosis factor. J. Exp. Med. 187:1477–1485.
  • Wang, Q., Wang X., and Evers B. M.. 2003. Induction of cIAP-2 in human colon cancer cells through PKCδ/NF-κB. J. Biol. Chem. 278:51091–51099.
  • Webster, J. C., Huber R. M., Hanson R. L., Collier P. M., Haws T. F., Mills J. K., Burn T. C., and Allegretto E. A.. 2002. Dexamethasone and tumor necrosis factor-alpha act together to induce the cellular inhibitor of apoptosis-2 gene and prevent apoptosis in a variety of cell types. Endocrinology 143:3866–3874.
  • Wen, L. P., Madani K., Martin G. A., and Rosen G. D.. 1998. Proteolytic cleavage of Ras GTPase activating protein during apoptosis. Cell Death Differ. 5:729–734.
  • Wendel, H. G., De Stanchina E., Fridman J. S., Malina A., Ray S., Kogan S., Cordon-Cardo C., Pelletier J., and Lowe S. W.. 2004. Survival signalling by Akt and eIF4E in oncogenesis and cancer therapy. Nature 428:332–337.
  • Widmann, C., Dolci W., and Thorens B.. 1995. Agonist-induced internalization and recycling of the glucagon-like peptide-1 receptor in transfected fibroblasts and in insulinomas. Biochem. J. 310:203–214.
  • Widmann, C., Gibson S., and Johnson G. L.. 1998. Caspase dependent cleavage of signaling proteins during apoptosis. A turn-off mechanism for anti-apoptotic signals. J. Biol. Chem. 273:7141–7147.
  • Widmann, C., Lassignal Johnson N., Gardner A. M., Smith R. J., and Johnson G. L.. 1997. Potentiation of apoptosis by low dose stress stimuli in cells expressing activated MEK kinase 1. Oncogene 15:2439–2447.
  • Xia, Z., Dickens M., Raingeaud J., Davis R. J., and Greenberg M. E.. 1995. Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis. Science 270:1326–1331.
  • Yang, J.-Y., and Widmann C.. 2001. Antiapoptotic signaling generated by caspase induced cleavage of RasGAP. Mol. Cell. Biol. 21:5346–5358.
  • Yang, J.-Y., and Widmann C.. 2002. A subset of caspase substrates functions as the Jekyll and Hyde of apoptosis. Eur. Cytokine Netw. 13:387.
  • Yang, J.-Y., and Widmann C.. 2002. The RasGAP N-terminal fragment generated by caspase cleavage protects cells in a Ras/PI3K/Akt-dependent manner that does not rely on NFκB activation. J. Biol. Chem. 277:14641–14646.
  • Yang, W., Guastella J., Huang J. C., Wang Y., Zhang L., Xue D., Tran M., Woodward R., Kasibhatla S., Tseng B., Drewe J., and Cai S. X.. 2003. MX1013, a dipeptide caspase inhibitor with potent in vivo antiapoptotic activity. Br. J. Pharmacol.
  • Yue, Y., Lypowy J., Hedhli N., and Abdellatif M.. 2004. Ras GTPase activating protein binds to Akt and is required for its activation. J. Biol. Chem. 279:12883–12889.

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