ArticleProceedings of the National Academy of Sciences of the United States of America1998
Synthetic activation of caspases: artificial death switches.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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.
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Who cites it
67 citing papers in PubMed, 187 citations in OpenAlex.
- Small-molecule control of CAR T cells.Nature reviews. Chemistry · 2025Review
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- Synthetic Biology Meets CaCells · 2024Review
- Engineering the next generation of theranostic biomaterials with synthetic biology.Bioactive materials · 2024Review
- Rewiring cancer drivers to activate apoptosis.Nature · 2023Article
- NLRP11 is a pattern recognition receptor for bacterial lipopolysaccharide in the cytosol of human macrophages.Science immunology · 2023Article
- Strategies for Conditional Regulation of Proteins.JACS Au · 2023Review
- Combinatorial suicide gene strategies for the safety of cell therapies.Frontiers in immunology · 2022Article
- Increased Susceptibility of the CD57International journal of molecular sciences · 2021Article
- The intricate biophysical puzzle of caspase-1 activation.Archives of biochemistry and biophysics · 2021Review
- The Role of Caspase-2 in Regulating Cell Fate.Cells · 2020Review
- Versatile cell ablation tools and their applications to study loss of cell functions.Cellular and molecular life sciences : CMLS · 2019Review
- Cancer cell killing by target antigen engagement with engineered complementary intracellular antibody single domains fused to pro-caspase3.Scientific reports · 2019Article
- Cucurbit[8]uril Reactivation of an Inactivated Caspase-8 Mutant Reveals Differentiated Enzymatic Substrate Processing.Chembiochem : a European journal of chemical biology · 2018Article
- Chemically induced proximity in biology and medicine.Science (New York, N.Y.) · 2018Review
- Glycolysis promotes caspase-3 activation in lipid rafts in T cells.Cell death & disease · 2018Article
- Exploiting Cell Death Pathways for Inducible Cell Elimination to Modulate Graft-versus-Host-Disease.Biomedicines · 2017Review
- Caspase-9: structure, mechanisms and clinical application.Oncotarget · 2017Review
- Inducible Caspase-9 Selectively Modulates the Toxicities of CD19-Specific Chimeric Antigen Receptor-Modified T Cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- Antioxidative and Antiapoptotic Effects of Delta-Opioid Peptide [D-AlaFrontiers in neuroscience · 2017Article
7 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
3 authors at 1 institution in 1 country.
Funding
Abstract
The development of safe vectors for gene therapy requires fail-safe mechanisms to terminate therapy or remove genetically altered cells. The ideal "suicide switch" would be nonimmunogenic and nontoxic when uninduced and able to trigger cell death independent of tissue type or cell cycle stage. By using chemically induced dimerization, we have developed powerful death switches based on the cysteine proteases, caspase-1 ICE (interleukin-1beta converting enzyme) and caspase-3 YAMA. In both cases, aggregation of the target protein is achieved by a nontoxic lipid-permeable dimeric FK506 analog that binds to the attached FK506-binding proteins, FKBPs. We find that intracellular cross-linking of caspase-1 or caspase-3 is sufficient to trigger rapid apoptosis in a Bcl-xL-independent manner, suggesting that these conditional proapoptotic molecules can bypass intracellular checkpoint genes, such as Bcl-xL, that limit apoptosis. Because these chimeric molecules are derived from autologous proteins, they should be nonimmunogenic and thus ideal for long-lived gene therapy vectors. These properties should also make chemically induced apoptosis useful for developmental studies, for treating hyperproliferative disorders, and for developing animal models to a wide variety of diseases.
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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.