Abstract
THE cell-killing effects of the cytokines TNF-α and FasL are mediated by the distinct cell-surface receptors TNFR1, TNFR2 and Fas (also known as CD95/APO-1), which are all members of a receptor superfamily that is important for regulating cell survival1–4. The cytoplasmic regions of TNFR1 and Fas contain a conserved 'death' domain which is an essential component of the signal pathway that triggers apoptosis and activation of the transcription factor NF-KB (refs 5, 6). Here we report the isolation of a 54K receptor that is a new member of the TNFR superfamily, using the death domain of TNFR1 in a yeast two-hybrid system7,8. This protein, WSL-1, is most similar to TNFR1 itself, particularly in the death-domain region. The gene wsl-1 is capable of inducing apoptosis when transfected into 3T3 and 293 cells, and can also activate NF-KB in 293 cells. Like TNFR1, WSL-1 will homodimerize in yeast. WSL-1 also interacts specifically with the TNFRl-associated molecule TRADD9. The tissue distribution is very restricted and significantly different from that of Fas and TNFR1.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 51 print issues and online access
$199.00 per year
only $3.90 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
Similar content being viewed by others
References
Vandenabeele, P., Declercq, W., Beyaert, R. & Fiers, W. Trends Cell Biol. 5, 392–399 (1995).
Baker, S. J. & Reddy, P. Oncogene 12, 1–9 (1996).
Zheng, L. et al. Nature 377, 348–351 (1995).
Smith, C. A., Farrah, T. & Goodwin, R. G. Cell 76, 959–962 (1994).
Tartaglia, L. A., Ayres, T. M., Wong, G. H. W. & Goeddel, D. V. Cell 74, 845–853 (1993).
Itoh, N. & Nagata, S. J. Biol. Chem. 268, 10932–10937 (1993).
Durfee, T. et al. Genes Dev. 7, 555–659 (1993).
Fields, S. & Song, O. Nature 340, 245–246 (1989).
Hsu, H., Xiong, J. & Goeddel, D. V. Cell 81, 495–504 (1995).
Boldin, M. P. et al. J. Biol. Chem. 270, 387–391 (1995).
Song, H. Y., Dunbar, J. D. & Bonner, D. B. J. Biol. Chem. 269, 22492–22495 (1994).
Wiegman, K., Schutz, E., Machleid, T. T., Witte, D. & Kronke, M. Cell 78, 1005–1015 (1994).
Chinnaiyan, A. M., O'Rourke, K., Tewari, M. & Dixit, V. M. Cell 81, 505–512 (1995).
Boldin, M. P. et al. J. Biol. Chem. 270, 7795–7798 (1995).
Stanger, B. Z., Leder, D., Lee, T.-H., Kim, E. & Seed, B. Cell 81, 513–523 (1995).
Cao, Z., Xiong, J., Takeuchi, M., Kurama, T. & Goeddel, D. V. Nature 383, 443–446 (1996).
Wiley, S. R. et al. Immunity 3, 673–682 (1995).
Nagata, S. & Golstein, P. Science 267, 1449–1456 (1995).
Ward, A. C. Nucleic Acids Res. 18, 5319 (1990).
Frohman, M. A., Dash, M. K. & Martin, G. R. Proc. Natl Acad. Sci. USA 85, 8998–9002 (1988).
Hsu, H., Shu, H.-B., Pan, M.-G. & Goeddel, D. V. Cell 84, 299–308 (1996).
Hsu, H., Huang, J., Shu, H.-B., Baichwal, V. & Goeddel, D. V. Immunity 4, 387–396 (1996).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Kitson, J., Raven, T., Jiang, YP. et al. A death-domain-containing receptor that mediates apoptosis. Nature 384, 372–375 (1996). https://doi.org/10.1038/384372a0
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1038/384372a0
This article is cited by
-
Direct signaling of TL1A-DR3 on fibroblasts induces intestinal fibrosis in vivo
Scientific Reports (2020)
-
Inflammation-independent TL1A-mediated intestinal fibrosis is dependent on the gut microbiome
Mucosal Immunology (2018)
-
TL1-A can engage death receptor-3 and activate NF-kappa B in endothelial cells
BMC Nephrology (2014)
-
Understanding the conservation patterns and molecular phylogenetics of human death receptors family through computational biology
3 Biotech (2014)
-
Expression and function of vascular endothelial growth inhibitor in aged porcine bladder detrusor muscle cells
Biogerontology (2013)
Comments
By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.
