Evidence map›Paper›PMID 28903044›Full record

ArticleCell reports2017

Engineering Synthetic Signaling Pathways with Programmable dCas9-Based Chimeric Receptors.

Toni A Baeumler, Ahmed Ashour Ahmed, Tudor A Fulga

Abstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Synthetic Gene Circuits for Regulation of Next-Generation Cell-Based Therapeutics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  10. Review
  11. Article
  12. Article
  13. Applications of synthetic biology in medical and pharmaceutical fields.Signal transduction and targeted therapy · 2023
    Review
  14. Article
  15. The evolution of synthetic receptor systems.Nature chemical biology · 2022
    Review
  16. Review
  17. Article
  18. Review
  19. Controlling and enhancing CRISPR systems.Nature chemical biology · 2021
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Toni A BaeumlerWeatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 9DS, UK.
Ahmed Ashour AhmedOvarian Cancer Cell Laboratory, Weatherall Institute of Molecular Medicine, Nuffield Department of Obstetrics and Gynaecology, University of Oxford, Oxford OX3 9DU, UK.
Tudor A FulgaWeatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 9DS, UK. Electronic address: tudor.fulga@imm.ox.ac.uk.

Funding

Medical Research Council G0902418
6 · The paper itself

Abstract

Synthetic receptors provide a powerful experimental tool for generation of designer cells capable of monitoring the environment, sensing specific input signals, and executing diverse custom response programs. To advance the promise of cellular engineering, we have developed a class of chimeric receptors that integrate a highly programmable and portable nuclease-deficient CRISPR/Cas9 (dCas9) signal transduction module. We demonstrate that the core dCas9 synthetic receptor (dCas9-synR) architecture can be readily adapted to various classes of native ectodomain scaffolds, linking their natural inputs with orthogonal output functions. Importantly, these receptors achieved stringent OFF/ON state transition characteristics, showed agonist-mediated dose-dependent activation, and could be programmed to couple specific disease markers with diverse, therapeutically relevant multi-gene expression circuits. The modular dCas9-synR platform developed here provides a generalizable blueprint for designing next generations of synthetic receptors, which will enable the implementation of highly complex combinatorial functions in cellular engineering.

Indexed as

Genetic EngineeringSignal TransductionCell MembraneCRISPR-Cas SystemsGene ExpressionHEK293 CellsHumansModels, BiologicalPeptide HydrolasesReceptors, G-Protein-CoupledRecombinant ProteinsTranscriptional ActivationTranscription FactorsPeptide HydrolasesReceptors, G-Protein-CoupledRecombinant ProteinsTranscription Factorschimeric receptorsCRISPRdCas9-synRdCas9-VP64genome engineeringGPCRRTKsplit Cas9synthetic receptorstranscriptional programs

Identifiers

PMID28903044
PMCPMC5608971

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.