Evidence map›Paper›PMID 30013045›Full record

ArticleNature methods2018

An enhanced CRISPR repressor for targeted mammalian gene regulation.

Nan Cher Yeo, Alejandro Chavez, Alissa Lance-Byrne, Yingleong Chan, David Menn, Denitsa Milanova, Chih-Chung Kuo, Xiaoge Guo, Sumana Sharma, Angela Tung and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature methods, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 300 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
300citing papers in PubMed, 1 pooled it
–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

300 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Mechanisms, Microenvironments, and Models: Understanding Therapeutic Resistance in Glioblastoma.International journal of radiation oncology, biology, physics · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Advances and clinical potential of epigenome editing.Cellular and molecular life sciences : CMLS · 2026
    Review
  15. Article
  16. Article
  17. Clinical translation of epigenome editing technologies.Current opinion in biomedical engineering · 2026
    Article
  18. Article
  19. Article
  20. Article

240 more citing papers are in PubMed but not listed here.

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

20 authors.

Nan Cher YeoWyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA.ORCID http://orcid.org/0000-0002-6354-4115
Alejandro ChavezDepartment of Pathology and Cell Biology, Columbia University College of Physicians and Surgeons, New York, NY, USA. ac4304@cumc.columbia.edu.ORCID http://orcid.org/0000-0001-5626-7140
Alissa Lance-ByrneWyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA.
Yingleong ChanWyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA.
David MennSchool of Biological and Health Systems Engineering, Ira A. Fulton Schools of Engineering, Arizona State University, Tempe, AZ, USA.
Denitsa MilanovaWyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA.
Chih-Chung KuoDepartment of Bioengineering, University of California, San Diego, San Diego, CA, USA.
Xiaoge GuoWyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA.
Sumana SharmaCell Surface Signalling Laboratory, Wellcome Trust Sanger Institute, Cambridge, UK.
Angela TungWyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA.
Ryan J CecchiWyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA.
Marcelle TuttleWyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA.
Swechchha PradhanSchool of Biological and Health Systems Engineering, Ira A. Fulton Schools of Engineering, Arizona State University, Tempe, AZ, USA.
Elaine T LimWyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA.
Noah DavidsohnWyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA.
Mo R EbrahimkhaniSchool of Biological and Health Systems Engineering, Ira A. Fulton Schools of Engineering, Arizona State University, Tempe, AZ, USA.
James J CollinsWyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA.
Nathan E LewisDepartment of Bioengineering, University of California, San Diego, San Diego, CA, USA.ORCID http://orcid.org/0000-0001-7700-3654
Samira KianiSchool of Biological and Health Systems Engineering, Ira A. Fulton Schools of Engineering, Arizona State University, Tempe, AZ, USA. samira.Kiani@asu.edu.ORCID http://orcid.org/0000-0003-2695-1501
George M ChurchWyss Institute for Biologically Inspired Engineering, Harvard University, Cambridge, MA, USA. gchurch@genetics.med.harvard.edu.ORCID http://orcid.org/0000-0003-3535-2076

Funding

Causal Transcriptional Consequences of Human Genetic VariationP50HG005550 · NHGRI · HARVARD MEDICAL SCHOOL · PI CHURCH, GEORGE M · 2010 to 2014
$19.0M
MOLECULAR IMMUNOLOGY AND TUMOR BIOLOGYT32CA009216 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI David Michael Langenau · 1985 to 2026
$10.6M
Center for Genomically Engineered OrgansRM1HG008525 · NHGRI · HARVARD MEDICAL SCHOOL · PI CHURCH, GEORGE M · 2015 to 2019
$10.2M
Unraveling the mammalian secretory pathway through systems biology and algorithm developmentR35GM119850 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LEWIS, NATHAN ENOCH · 2016 to 2025
$4.3M
NCI NIH HHS T32 CA009216NHGRI NIH HHS P50 HG005550NHGRI NIH HHS RM1 HG008525NIGMS NIH HHS R35 GM119850
6 · The paper itself

Abstract

The RNA-guided endonuclease Cas9 can be converted into a programmable transcriptional repressor, but inefficiencies in target-gene silencing have limited its utility. Here we describe an improved Cas9 repressor based on the C-terminal fusion of a rationally designed bipartite repressor domain, KRAB-MeCP2, to nuclease-dead Cas9. We demonstrate the system's superiority in silencing coding and noncoding genes, simultaneously repressing a series of target genes, improving the results of single and dual guide RNA library screens, and enabling new architectures of synthetic genetic circuits.

Indexed as

CRISPR-Cas SystemsGene Expression RegulationGene SilencingCRISPR-Associated Protein 9Genes, SyntheticHEK293 CellsHumansMethyl-CpG-Binding Protein 2Recombinant Fusion ProteinsRepressor ProteinsRNA, Guide, CRISPR-Cas SystemsCRISPR-Associated Protein 9MECP2 protein, humanMethyl-CpG-Binding Protein 2Recombinant Fusion ProteinsRepressor ProteinsRNA, Guide, CRISPR-Cas Systems

Identifiers

PMID30013045
PMCPMC6129399

What OpenQuestion holds

Textmetadata
LicenceTDM
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.