ArticleOncogene2001
Differential activation of TRAIL-R1 and -2 by soluble and membrane TRAIL allows selective surface antigen-directed activation of TRAIL-R2 by a soluble TRAIL derivative.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
85 citing papers in PubMed, 206 citations in OpenAlex.
- Jurkat T-Cell Antigen-Independent Elimination of PMA-Activated Neuroblastoma Cells Is Triggered by CCL2/CCR2, Depends Upon Lipid Raft LFA1/ICAM1 Immune Synapses, Is Mediated by m-TRAIL and Is Augmented by the TrkAIII Oncoprotein.International journal of molecular sciences · 2026Article
- Quercetin Increases Expression of Membrane-TRAIL in Glioblastoma Cells Resulting in Apoptosis.Cancers · 2025Article
- Comparative study of the anti-tumour effects of the imipridone, ONC201 and its fluorinated analogues on pancreatic cancer cell line.Scientific reports · 2025Article
- Comparison of antibody-scTRAIL Fc fusion proteins with varying valency for EGFR and TRAIL receptors.Scientific reports · 2025Article
- Turn TRAIL Into Better Anticancer Therapeutic Through TRAIL Fusion Proteins.Cancer medicine · 2025Review
- Review
- Tuning of TRAIL clustering on the surface of nanoscale liposomes by phase separation.Nanoscale advances · 2024Article
- Ionizable Lipid Nanoparticle-Mediated TRAIL mRNA Delivery in the Tumor Microenvironment to Inhibit Colon Cancer Progression.International journal of nanomedicine · 2024Article
- Regulation of anoikis by extrinsic death receptor pathways.Cell communication and signaling : CCS · 2023Review
- Exosomal delivery of TRAIL and miR‑335 for the treatment of hepatocellular carcinoma (Review).International journal of molecular medicine · 2023Review
- The benefits of clustering in TNF receptor superfamily signaling.Frontiers in immunology · 2023Review
- TRAIL and its receptors in cardiac diseases.Frontiers in physiology · 2023Review
- Lipid Phase Separation in Vesicles Enhances TRAIL-Mediated Cytotoxicity.Nano letters · 2022Article
- NCTRCancer chemotherapy and pharmacology · 2021Article
- Engineering of CD19 Antibodies: A CD19-TRAIL Fusion Construct Specifically Induces Apoptosis in B-Cell Precursor Acute Lymphoblastic Leukemia (BCP-ALL) Cells In Vivo.Journal of clinical medicine · 2021Article
- Review
- Overcoming TRAIL Resistance for Glioblastoma Treatment.Biomolecules · 2021Review
- Review
- Molecular imaging of fibroblast activation protein after myocardial infarction using the novel radiotracer [Theranostics · 2021Article
- The Neutrophil: The Underdog That Packs a Punch in the Fight against Cancer.International journal of molecular sciences · 2020Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TNF-related apoptosis-inducing ligand (TRAIL) is a typical member of the tumor necrosis factor (TNF) ligand family that is expressed as a type II membrane protein (memTRAIL) and signals apoptosis via the death domain-containing receptors TRAIL-R1 and -2. Soluble recombinant derivatives of TRAIL (sTRAIL) are considered as novel tumors therapeutics because of their selective apoptosis inducing activity in a variety of human tumors but not in normal cells. Using antagonistic antigen-binding fragment (Fab) preparations of TRAIL-R1- and TRAIL-R2-specific antibodies, we demonstrate in this study that TRAIL-R1 becomes activated by both the soluble and the membrane-bound form of the ligand, whereas TRAIL-R2 becomes only activated by memTRAIL or soluble TRAIL secondarily cross-linked by antibodies. Furthermore, we show that the restricted signal capacity of sTRAIL can be readily converted into a fully signal competent memTRAIL-like molecule, i.e. a TRAIL-R2 stimulating ligand, by genetic fusion to an antibody derivative that allows antigen-dependent 'immobilization' of the fusion protein to cell surfaces. We conclude that antibody targeting-dependent activation can be used to design selective therapeutics derived of those ligands of the TNF family that are biologically inactive in their soluble form.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.