The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-xL
Open accessAbstract
Fas activation triggers apoptosis in many cell types. Studies with anti-Fas antibodies have produced conflicting results on Fas signaling, particularly the role of the Bcl-2 family in this process. Comparison between physiological ligand and anti-Fas antibodies revealed that only extensive Fas aggregation, by membrane bound FasL or aggregated soluble FasL consistently triggered apoptosis, whereas antibodies could act as death agonists or antagonists. Studies on Fas signaling in cell lines and primary cells from transgenic mice revealed that FADD/MORT1 and caspase-8 were required for apoptosis. In contrast, Bcl-2 or Bcl-x L did not block FasL-induced apoptosis in lymphocytes or hepatocytes, demonstrating that signaling for cell death induced by Fas and the pathways to apoptosis regulated by the Bcl-2 family are distinct.
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Cites
Death Receptors: Signaling and Modulation
Ashkenazi, A., & Dixit, V. M. (1998) · Science · doi:10.1126/science.281.5381.1305 · Cited by 5,866
Boldin, M. P., Varfolomeev, E. E., Pancer, Z., Mett, I. L., Camonis, J. H., & Wallach, D. (1995) · Journal of Biological Chemistry · doi:10.1074/jbc.270.14.7795 · Cited by 993
Cited by
Apo2L/TRAIL-Dependent Recruitment of Endogenous FADD and Caspase-8 to Death Receptors 4 and 5
Kischkel, F. C., Lawrence, D. A., Chuntharapai, A., Schow, P., Kim, K. J., & Ashkenazi, A. (2000) · Immunity · doi:10.1016/s1074-7613(00)80212-5 · Cited by 975
The many roles of FAS receptor signaling in the immune system
Strasser, A., Jost, P. J., & Nagata, S. (2009) · Immunity · doi:10.1016/j.immuni.2009.01.001 · Cited by 968
Self-citationKazama, H., Ricci, J.-E., Herndon, J. M., Hoppe, G., Green, D. R., & Ferguson, T. A. (2008) · Immunity · doi:10.1016/j.immuni.2008.05.013 · Cited by 627
XIAP discriminates between type I and type II FAS-induced apoptosis
Jost, P. J., Grabow, S., Gray, D., McKenzie, M. D., Nachbur, U., Huang, D. C. S., Bouillet, P., Thomas, H. E., Borner, C., Silke, J., et al. (2009) · Nature · doi:10.1038/nature08229 · Cited by 482
Self-citationBarnhart, B. C., Alappat, E. C., & Peter, M. E. (2003) · Seminars in Immunology · doi:10.1016/s1044-5323(03)00031-9 · Cited by 419
Metadata
- Authors
- Huang, D. C. S., Hahne, M., Schroeter, M., Frei, K., Fontana, A., Villunger, A., Newton, K., Tschopp, J., & Strasser, A.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1999-12-21
- Volume
- 96
- Issue
- 26
- Pages
- 14871-14876
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1996174406
- Cited by
- 297
- References
- 2
- FWCI
- 10.22
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-xL. https://app.cochat.ai/papers/10.1073/pnas.96.26.14871
- The paper
- Huang, D. C. S., Hahne, M., Schroeter, M., Frei, K., Fontana, A., Villunger, A., Newton, K., Tschopp, J., & Strasser, A. (1999). Activation of Fas by FasL induces apoptosis by a mechanism that cannot be blocked by Bcl-2 or Bcl-xL. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.96.26.14871
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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