CoChat
Sign Up
Cited by 102Cell death mechanisms and regulationCancer-related Molecular PathwaysToxin Mechanisms and Immunotoxins

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

French, Lars E, Tschopp, Jürg·2003·Cell Death & Differentiation
DOI 10.1038/sj.cdd.4401185
Open this paper in CoChat — free account

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.

Overview

Integrity signals

Registry

Crossref · 10.1038/sj.cdd.4401185

Cites

50 of 50 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Cited by

Sorted by citations

See all 102

Related

See all

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
Publisher
Springer Science and Business Media LLC
Published
2003-01
Volume
10
Issue
1
Pages
117-123
ISSN
  • 1350-9047 (ISSN-L)
  • 1476-5403
DOI
10.1038/sj.cdd.4401185
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review