Evidence map›Paper›PMID 29235474›Full record

ArticleNature communications2017

Engineering cell signaling using tunable CRISPR-Cpf1-based transcription factors.

Yuchen Liu, Jinghong Han, Zhicong Chen, Hanwei Wu, Hongsong Dong, Guohui Nie

Open access · goldAbstract read
In one paragraph

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 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.7field-weighted citation impact, top 4% of its field
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

58 citing papers in PubMed, 122 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. HyperCas12a enables multiplexed CRISPRi screens.bioRxiv : the preprint server for biology · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Pooled screening with next-generation gene editing tools.Current opinion in biomedical engineering · 2023
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. A CRISPR-Cas Cure for HIV/AIDS.International journal of molecular sciences · 2023
    Review
  18. Review
  19. Article
  20. Review
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

6 authors at 1 institution in 1 country.

Yuchen LiuInstitute of Translational Medicine, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, 518039, China.
Jinghong HanInstitute of Translational Medicine, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, 518039, China.
Zhicong ChenInstitute of Translational Medicine, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, 518039, China.
Hanwei WuInstitute of Translational Medicine, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, 518039, China.
Hongsong DongDepartment of Otolaryngology, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, 518039, China.
Guohui NieInstitute of Translational Medicine, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, 518039, China. nghui@21cn.com.
Shenzhen Second People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The catalytically dead Cpf1 endonuclease from Acidaminococcus sp. BV3L6 (dAsCpf1) has been used to construct effective transcriptional repressors in bacteria and plants. However, it is still unclear if dAsCpf1 can function in human cells as a transcriptional regulator or a signal conductor. Here, we repurpose the dAsCpf1 system in human cells for a variety of functions, including the activation or repression of gene transcription. Moreover, we construct programmable ligand-controlled dAsCpf1 systems either by coupling crRNAs with engineered riboswitches or by fusing dAsCpf1 proteins with G protein-coupled receptors. These generalizable approaches allow us to regulate the transcription of endogenous genes in response to diverse classes of ligands, thus constructing artificial signaling pathways with rewired cellular input-output behaviors. The systems exhibit signal amplification, an important feature in cell signaling, when multiple crRNAs are processed from a single transcript. The results provide a robust and efficient platform for engineering customized cell signaling circuits.

Indexed as

CRISPR-Cas SystemsBacterial ProteinsCell EngineeringCRISPR-Associated ProteinsEndodeoxyribonucleasesEndonucleasesGene EditingGene Expression RegulationHEK293 CellsHeLa CellsHumansReceptors, G-Protein-CoupledSignal TransductionTranscription FactorsBacterial ProteinsCas12a proteinCRISPR-Associated ProteinsEndodeoxyribonucleasesEndonucleasesReceptors, G-Protein-CoupledTranscription Factors

Identifiers

PMID29235474
PMCPMC5727435
OpenAlexW2774262345

What OpenQuestion holds

Textmetadata
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.