ArticleNature communications2017
Development of a genetic sensor that eliminates p53 deficient cells.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Cucurbitacin B Inhibits the Proliferation of WPMY-1 Cells and HPRF Cells via the p53/MDM2 Axis.International journal of molecular sciences · 2024Article
- Synthetic biology approaches for improving the specificity and efficacy of cancer immunotherapy.Cellular & molecular immunology · 2024Review
- Single-cell analysis of matrisome-related genes in breast invasive carcinoma: new avenues for molecular subtyping and risk estimation.Frontiers in immunology · 2024Article
- Precise tumor immune rewiring via synthetic CRISPRa circuits gated by concurrent gain/loss of transcription factors.Nature communications · 2022Article
- Immunoregulatory framework and the role of miRNA in the pathogenesis of NSCLC - A systematic review.Frontiers in oncology · 2022Review
- Recent Advances of Nanotechnology-Facilitated Bacteria-Based Drug and Gene Delivery Systems for Cancer Treatment.Pharmaceutics · 2021Review
- Synthesis of RNA-based gene regulatory devices for redirecting cellular signaling events mediated by p53.Theranostics · 2021Article
- A Light-Inducible Split-dCas9 System for Inhibiting the Progression of Bladder Cancer Cells by Activating p53 and E-cadherin.Frontiers in molecular biosciences · 2020Article
- Engineering Cellular Signal Sensors based on CRISPR-sgRNA Reconstruction Approaches.International journal of biological sciences · 2020Review
- Synthetic Biology Speeds Up Drug Target Discovery.Frontiers in pharmacology · 2020Review
- Engineering advanced cancer therapies with synthetic biology.Nature reviews. Cancer · 2019Review
- Combined treatment of cholangiocarcinoma with interventional radiofrequency hyperthermia and heat shock protein promoter-mediated HSV-TK gene therapy.American journal of cancer research · 2018Article
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Authors and funding
5 authors.
Funding
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Abstract
The TP53 gene fulfills a central role in protecting cells from genetic insult. Given this crucial role it might be surprising that p53 itself is not essential for cell survival. Indeed, TP53 is the single most mutated gene across different cancer types. Thus, both a theoretical and a question of significant practical applicability arise: can cells be programmed to make TP53 an essential gene? Here we present a genetic p53 sensor, in which the loss of p53 is coupled to the rise of HSV-TK expression. We show that the sensor can distinguish both p53 knockout and cells expressing a common TP53 cancer mutation from otherwise isogenic TP53 wild-type cells. Importantly, the system is sensitive enough to specifically target TP53 loss-of-function cells with the HSV-TK pro-drug Ganciclovir both in vitro and in vivo. Our work opens new ways to programming cell intrinsic transformation protection systems that rely on endogenous components.
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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.