The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index.
Protein-based therapeutic approaches targeting death receptors
Abstract
Death receptors (DRs) are a growing family of transmembrane proteins that can detect the presence of specific extracellular death signals and rapidly trigger cellular destruction by apoptosis. Eight human DRs (Fas, TNF-R1, TRAMP, TRAIL-R1, TRAIL-R2, DR-6, EDA-R and NGF-R) have been identified. The best studied to date is Fas (CD95). Expression and signaling by Fas and its ligand (FasL, CD95L) is a tightly regulated process essential for key physiological functions in a variety of organs, including the maintenance of immune homeostasis. Recently, strong evidence has shown that dysregulation of Fas expression and/or signaling contributes to the pathogenesis of tissue destructive diseases such as graft-versus-host disease, toxic epidermal necrolysis, multiple sclerosis and stroke. With these new developments, strategies for modulating the function of Fas signaling have emerged and provided novel protein-based therapeutic possibilities that will be discussed herein. Selective triggering of DR-mediated apoptosis in cancer cells is an emerging approach that is being intensely investigated as a mode of cancer therapy. Local administration of Fas agonists, and more promisingly, systemic use of soluble recombinant forms of TRAIL have shown efficacy in preclinical models of the disease. Developments in this field that may have important clinical implications for the treatment of cancer are reviewed.
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“FASLG has therefore been proposed as a therapeutic target for acute treatment of stroke [25].”
From MicroRNA‐21 protects neurons from ischemic death (2010) · cites this paper as [25]
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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
Tumoricidal activity of tumor necrosis factor-related apoptosis-inducing ligand in vivo.
Walczak, H., Miller, R. E., Ariail, K., Gliniak, B., Griffith, T. S., Kubin, M., Chin, W., Jones, J., Woodward, A., Le, T., et al. (1999) · Nature Medicine · doi:10.1038/5517 · Cited by 2,497
Safety and antitumor activity of recombinant soluble Apo2 ligand
Ashkenazi, A., Pai, R. C., Fong, S., Leung, S., Lawrence, D. A., Marsters, S. A., Blackie, C., Chang, L., McMurtrey, A. E., Hebert, A., et al. (1999) · Journal of Clinical Investigation · doi:10.1172/jci6926 · Cited by 2,213
Holler, N., Zaru, R., Micheau, O., Thome, M., Attinger, A., Valitutti, S., Bodmer, J.-L., Schneider, P., Seed, B., & Tschopp, J. (2000) · Nature Immunology · doi:10.1038/82732 · Cited by 1,987
Self-citationLethal effect of the anti-Fas antibody in mice
Ogasawara, J., Watanabe-Fukunaga, R., Adachi, M., Matsuzawa, A., Kasugai, T., Kitamura, Y., Itoh, N., Suda, T., & Nagata, S. (1993) · Nature · doi:10.1038/364806a0 · Cited by 1,881
Johnstone (2002) · doi:10.1016/s0092-8674(02)00625-6 · Cited by 1,876
Monoclonal Antibody-Mediated Tumor Regression by Induction of Apoptosis
Trauth, B. C., Klas, C., Peters, A. M. J., Matzku, S., Mӧller, P., Falk, W., Debatin, K., & Krammer, P. H. (1989) · Science · doi:10.1126/science.2787530 · Cited by 1,716
Apoptosis control by death and decoy receptors
Ashkenazi, A., & Dixit, V. M. (1999) · Current Opinion in Cell Biology · doi:10.1016/s0955-0674(99)80034-9 · Cited by 1,281
Inhibition of Toxic Epidermal Necrolysis by Blockade of CD95 with Human Intravenous Immunoglobulin
Viard, I., Wehrli, P., Bullani, R. R., Schneider, P., Holler, N., Salomon, D., Hunziker, T., Saurat, J. ‐., Tschopp, J., & French, L. E. (1998) · Science · doi:10.1126/science.282.5388.490 · Cited by 1,000
Self-citationInhibition of toxic epidermal necrolysis by blockade of CD95 with human intravenous immunoglobulin
(1999) · Transfusion Medicine Reviews · doi:10.1016/s0887-7963(99)80071-6 · Cited by 871
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Delloye‐Bourgeois, C. (2011) · theses.fr (ABES) · doi:10.70675/4113065azf844z4aceza648z1b5c64df1f33
Molecular Analysis of the TRAIL DISC and its signalling pathways
Sprick, M. R. (2003) · KOPS (University of Konstanz)
Metadata
- Authors
- French, L. E., & Tschopp, J.
- Affiliations
- University of Geneva (CH)
- University of Lausanne (CH)
- Corresponding author
- French, Lars E
- ORCID
- French, Lars E
- Venue
- Cell Death & Differentiation
- Published
- 2003-01
- Volume
- 10
- Issue
- 1
- Pages
- 117-123
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- OpenAlex
- W2035127186
- Cited by
- 102
- References
- 50
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 6 · 2015: 9 · 2014: 4 · 2013: 3 · 2012: 6
- FWCI
- 0.78
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Death and Differentiation (publishedVersion)
- PubMed (publishedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Toxin Mechanisms and Immunotoxins
- Keywords
- death receptors, Fas, Fas ligand, TRAIL, TRAIL-R1, DR5, apoptosis, cancer therapy, immune homeostasis, graft-versus-host disease, toxic epidermal necrolysis, multiple sclerosis, stroke, therapeutic proteins
- MeSH terms
- Animals, Antineoplastic Agents, Eukaryotic Cells, Humans, Membrane Glycoproteins, Neoplasms, Tumor Necrosis Factor-alpha, Apoptosis, fas Receptor, Apoptosis Regulatory Proteins, TNF-Related Apoptosis-Inducing Ligand, Fas Ligand Protein
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