Evidence map›Paper›PMID 32316223›Full record

ReviewCells2020

CRISPR/Cas9 Epigenome Editing Potential for Rare Imprinting Diseases: A Review.

Linn Amanda Syding, Petr Nickl, Petr Kasparek, Radislav Sedlacek

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Expanding the CRISPR/Cas toolkit: applications in proteomics and theranostics.Frontiers in bioengineering and biotechnology · 2025
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Ablation ofGenes · 2023
    Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Epigenetics, microRNA and Metabolic Syndrome: A Comprehensive Review.International journal of molecular sciences · 2021
    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

4 authors at 1 institution in 1 country.

Linn Amanda SydingLaboratory of Transgenic Models of Diseases, Institute of Molecular Genetics of the CAS, v.v.i, 252 50 Vestec, Czech Republic.
Petr NicklLaboratory of Transgenic Models of Diseases, Institute of Molecular Genetics of the CAS, v.v.i, 252 50 Vestec, Czech Republic.
Petr KasparekLaboratory of Transgenic Models of Diseases, Institute of Molecular Genetics of the CAS, v.v.i, 252 50 Vestec, Czech Republic.
Radislav SedlacekLaboratory of Transgenic Models of Diseases, Institute of Molecular Genetics of the CAS, v.v.i, 252 50 Vestec, Czech Republic.
Czech Academy of Sciences, Institute of Molecular Genetics · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Imprinting diseases (IDs) are rare congenital disorders caused by aberrant dosages of imprinted genes. Rare IDs are comprised by a group of several distinct disorders that share a great deal of homology in terms of genetic etiologies and symptoms. Disruption of genetic or epigenetic mechanisms can cause issues with regulating the expression of imprinted genes, thus leading to disease. Genetic mutations affect the imprinted genes, duplications, deletions, and uniparental disomy (UPD) are reoccurring phenomena causing imprinting diseases. Epigenetic alterations on methylation marks in imprinting control centers (ICRs) also alters the expression patterns and the majority of patients with rare IDs carries intact but either silenced or overexpressed imprinted genes. Canonical CRISPR/Cas9 editing relying on double-stranded DNA break repair has little to offer in terms of therapeutics for rare IDs. Instead CRISPR/Cas9 can be used in a more sophisticated way by targeting the epigenome. Catalytically dead Cas9 (dCas9) tethered with effector enzymes such as DNA de- and methyltransferases and histone code editors in addition to systems such as CRISPRa and CRISPRi have been shown to have high epigenome editing efficiency in eukaryotic cells. This new era of CRISPR epigenome editors could arguably be a game-changer for curing and treating rare IDs by refined activation and silencing of disturbed imprinted gene expression. This review describes major CRISPR-based epigenome editors and points out their potential use in research and therapy of rare imprinting diseases.

Indexed as

CRISPR-Cas SystemsAngelman SyndromeDiabetes MellitusDNA MethylationEpigenesis, GeneticEpigenomeGene EditingGenomic ImprintingHumansInfant, Newborn, DiseasesPrader-Willi SyndromeRare DiseasesSilver-Russell SyndromeAngelman syndromeCRISPR/Cas9epigenome editinggenomic imprintingPrader-Willi syndromerare diseaseSilver-Russell syndrometranscriptome editingtransient neonatal diabetes mellitus

Identifiers

PMID32316223
PMCPMC7226972
OpenAlexW3017126064

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.