Evidence map›Paper›PMID 35977479›Full record

ArticleCell reports2022

Negative autoregulation mitigates collateral RNase activity of repeat-targeting CRISPR-Cas13d in mammalian cells.

Chase P Kelley, Maja C Haerle, Eric T Wang

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.9field-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

34 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. A Modular and Programmable Cas13d Platform for RNA Single Nucleotide Variant Detection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  7. Article
  8. Article
  9. Precise RNA targeting with CRISPR-Cas13d.Nature biotechnology · 2026
    Article
  10. Review
  11. Article
  12. Leveraging CRISPR-Cas13d in an inducible knockdown system to interrogatebioRxiv : the preprint server for biology · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Enhanced RNA-targeting CRISPR-Cas technology in zebrafish.bioRxiv : the preprint server for biology · 2024
    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 at 1 institution in 1 country.

Chase P KelleyDepartment of Molecular Genetics & Microbiology, Center for NeuroGenetics, Genetics Institute, University of Florida, Gainesville, FL 32608, USA; Genetics and Genomics Graduate Program, University of Florida, Gainesville, FL 32608, USA.
Maja C HaerleDepartment of Molecular Genetics & Microbiology, Center for NeuroGenetics, Genetics Institute, University of Florida, Gainesville, FL 32608, USA.
Eric T WangDepartment of Molecular Genetics & Microbiology, Center for NeuroGenetics, Genetics Institute, University of Florida, Gainesville, FL 32608, USA; Myology Institute, University of Florida, Gainesville, FL 32608, USA. Electronic address: eric.t.wang@ufl.edu.
University of Florida · US

Funding

Training and Educational CoreU54NS048843 · NINDS · UNIVERSITY OF ROCHESTER · PI THORNTON, CHARLES A · 2003 to 2017
$21.9M
Senator Paul D. Wellstone Muscular Dystrophy Specialized Research CenterP50NS048843 · NINDS · UNIVERSITY OF ROCHESTER · PI THORNTON, CHARLES A · 2018 to 2022
$7.1M
Impeding transcription of expanded microsatellite repeats using deactivated Cas9R01AG058636 · NIA · UNIVERSITY OF FLORIDA · PI WANG, ERIC T · 2019 to 2023
$1.9M
NIA NIH HHS R01 AG058636NINDS NIH HHS P50 NS048843NINDS NIH HHS U54 NS048843
6 · The paper itself

Abstract

CRISPR-Cas13 RNA endonucleases show promise for programmable RNA knockdown. However, sequence-specific binding of Cas13 unleashes non-specific bystander RNA cleavage, or collateral activity, raising concerns for experiments and therapeutic applications. Although robust in cell-free and bacterial environments, collateral activity in mammalian cells remains disputed. We investigate Cas13d collateral activity in a therapeutic context for myotonic dystrophy type 1, caused by a transcribed CTG repeat expansion. We find that, when targeting CUG

Indexed as

Gene EditingMyotonic DystrophyAnimalsCRISPR-Cas SystemsHomeostasisHumansMammalsRibonucleasesRNARNA, Guide, CRISPR-Cas SystemsRibonucleasesRNARNA, Guide, CRISPR-Cas SystemsCas13dcollateral activityCP: Molecular biologyCRISPRDM1gene therapyGENOgRNA excisionmyotonic dystrophynegative autoregulationrepeat expansion disease

Identifiers

PMID35977479
PMCPMC9809062
OpenAlexW4292055839

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.