Loss of TRAIL-R does not affect thymic or intestinal tumor development in p53 and adenomatous polyposis coli mutant mice (original) (raw)

Cell Death & Differentiation volume 12, pages 94–97 (2005)Cite this article

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TRAIL (TNF-Related Apoptosis-Inducing Ligand) and the TRAIL receptors were originally isolated based to their homology to tumor necrosis factor (TNF) and TNF receptor (TNFR) family members.1, 2, 3 In humans, five TRAIL receptors have been characterized. Two of these receptors, DR4 and DR5, contain an intracellular protein motif known as a death domain, which can transmit an apoptotic signal. Two additional receptors, DcR1 and DcR2, lack a functional death domain and appear to function as decoy receptors to inhibit signaling by TRAIL.4 The fifth receptor, osteoprotegerin (OPG), has been shown to bind TRAIL in vitro but has low affinity for the ligand at physiological temperatures;5 therefore, it is unclear as to whether it is a true receptor for TRAIL. In mice, one full length signaling receptor (TRAIL-R) and two decoy receptors lacking death domains have been identified.6, 7 Like Fas and TNFR, TRAIL-R induces apoptosis in a broad range of transformed cell lines in a FADD- and caspase-8-dependent manner.8, 9, 10, 11 In contrast to Fas and TNFR, most nontransformed cells are resistant to TRAIL-R-mediated death;1, 12, 13 as a result, there is considerable interest in the potential role of TRAIL as a cancer therapeutic.

References

  1. Wiley SR et al. (1995) Immunity 3: 673–682
  2. Pan G et al. (1997) Science 276: 111–113
  3. Pan G et al. (1997) Science 277: 815–818
  4. LeBlanc HN et al. (2003) Cell Death Differ. 10: 66–75
  5. Truneh A et al. (2000) J. Biol. Chem. 275: 23319–23325
  6. Wu GS et al. (1999) Cancer Res. 59: 2770–2775
  7. Schneider P et al. (2002) J. Biol. Chem. 278: 5444–5454
  8. Schneider P et al. (1997) FEBS Lett. 416: 329–334
  9. Kuang AA et al. (2000) J. Biol. Chem. 275: 25065–25068
  10. Kischkel FC et al. (2000) Immunity 12: 611–620
  11. Sprick MR et al. (2000) Immunity 12: 599–609
  12. Sheridan JP et al. (1997) Science 277: 818–821
  13. Walczak H et al. (1999) Nat. Med. 5: 157–163
  14. Mariani SM et al. (1998) Eur. J. Immunol. 28: 1492–1498
  15. Smyth MJ et al. (2001) J. Exp. Med. 193: 661–670
  16. Kayagaki N et al. (1999) J. Immunol. 162: 2639–2647
  17. Kayagaki N et al. (1999) J. Immunol. 163: 1906–1913
  18. Takeda K et al. (2001) Nat. Med. 7: 94–100
  19. Takeda K et al. (2002) J. Exp. Med. 195: 161–169
  20. Cretney E et al. (2002) J. Immunol. 168: 1356–1361
  21. Sedger LM et al. (2002) Eur. J. Immunol. 32: 2246–2254
  22. Jacks T et al. (1994) Curr. Biol. 4: 1–7
  23. Donehower LA et al. (1992) Nature 356: 215–221
  24. Harvey M et al. (1993) Nat. Genet. 5: 225–229
  25. Donehower LA et al. (1995) Mol. Carcinogen. 14: 16–22
  26. Wu GS et al. (1997) Nat. Genet. 17: 141–143
  27. Koornstra JJ et al. (2003) J. Pathol. 200: 327–335
  28. Mohr A et al. (2004) Gene Ther. 11: 534–543
  29. Moser AR et al. (1990) Science 247: 322–324
  30. Su LK et al. (1992) Science 256: 668–670
  31. Yang K et al. (1998) Cancer Res. 58: 5713–5717
  32. Moser AR et al. (1992) J. Cell Biol. 116: 1517–1526
  33. Luongo C et al. (1994) Cancer Res. 54: 5947–5952
  34. Groden J et al. (1991) Cell 66: 589–600

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Acknowledgements

We thank Kristina Hsieh for help in mouse husbandry and genotyping and James P Allison for helpful discussions about triangular mice. This work is supported by the National Institute of Health Grant CA92000 to AW. HHY is a National Science Foundation Predoctoral Research Fellow.

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  1. H H Yue and G E Diehl: These authors contributed equally to this work

Authors and Affiliations

  1. Cancer Research Laboratory and Department of Molecular and Cell Biology, University of California, Berkeley, CA, 94720-3200, USA
    H H Yue, G E Diehl & A Winoto

Authors

  1. H H Yue
  2. G E Diehl
  3. A Winoto

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Correspondence toA Winoto.

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Yue, H., Diehl, G. & Winoto, A. Loss of TRAIL-R does not affect thymic or intestinal tumor development in p53 and adenomatous polyposis coli mutant mice.Cell Death Differ 12, 94–97 (2005). https://doi.org/10.1038/sj.cdd.4401523

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