Evidence map›Paper›PMID 34935462›Full record

ArticleThe CRISPR journal2022

Chimeric RNA: DNA TracrRNA Improves Homology-Directed Repair

Brandon W Simone, Han B Lee, Camden L Daby, Hirotaka Ata, Santiago Restrepo-Castillo, Gabriel Martínez-Gálvez, Bibekananda Kar, William A C Gendron, Karl J Clark, Stephen C Ekker

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The CRISPR journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 50% 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

0 citing papers in PubMed, 5 citations in OpenAlex.

No citing paper in PubMed yet.

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

10 authors at 2 institutions in 1 country.

Brandon W SimoneDepartment of Biochemistry and Molecular Biology, Biomedical Engineering and Physiology Track, Mayo Clinic, Rochester, Minnesota, USA.
Han B LeeDepartment of Biochemistry and Molecular Biology, Biomedical Engineering and Physiology Track, Mayo Clinic, Rochester, Minnesota, USA.
Camden L DabyDepartment of Biochemistry and Molecular Biology, Biomedical Engineering and Physiology Track, Mayo Clinic, Rochester, Minnesota, USA.
Hirotaka AtaDepartment of Clinical and Translational Sciences, Biomedical Engineering and Physiology Track, Mayo Clinic, Rochester, Minnesota, USA.
Santiago Restrepo-CastilloMayo Clinic Graduate School of Biomedical Sciences, Virology and Gene Therapy Track, Biomedical Engineering and Physiology Track, Mayo Clinic, Rochester, Minnesota, USA.
Gabriel Martínez-GálvezMayo Clinic Graduate School of Biomedical Sciences, Biomedical Engineering and Physiology Track, Mayo Clinic, Rochester, Minnesota, USA.
Bibekananda KarDepartment of Biochemistry and Molecular Biology, Biomedical Engineering and Physiology Track, Mayo Clinic, Rochester, Minnesota, USA.
William A C GendronMayo Clinic Graduate School of Biomedical Sciences, Virology and Gene Therapy Track, Biomedical Engineering and Physiology Track, Mayo Clinic, Rochester, Minnesota, USA.
Karl J ClarkDepartment of Biochemistry and Molecular Biology, Biomedical Engineering and Physiology Track, Mayo Clinic, Rochester, Minnesota, USA.
Stephen C EkkerDepartment of Biochemistry and Molecular Biology, Biomedical Engineering and Physiology Track, Mayo Clinic, Rochester, Minnesota, USA.
Mayo Clinic · USMayo Clinic in Arizona · US

Funding

In vivo model of microglia inflammasome signaling in neuroinflammationR24OD020166 · OD · IOWA STATE UNIVERSITY · PI CLARK, KARL J, EKKER, STEPHEN CARL · 2016 to 2023
$7.1M
Conditional genetics and precision genome editing resources for ZebrafishR24OD036201 · OD · IOWA STATE UNIVERSITY · PI KARL J CLARK, Stephen Carl Ekker · 2024 to 2026
$3.0M
Development and genetics of rapid neuroendocrine stress responseR01GM134732 · NIGMS · MAYO CLINIC ROCHESTER · PI CLARK, KARL J · 2019 to 2022
$1.6M
NIGMS NIH HHS R01 GM134732NIH HHS R24 OD020166NIH HHS R24 OD036201
6 · The paper itself

Abstract

Nearly 90% of human pathogenic mutations are caused by small genetic variations, and methods to correct these errors efficiently are critically important. One way to make small DNA changes is providing a single-stranded oligo deoxynucleotide (ssODN) containing an alteration coupled with a targeted double-strand break (DSB) at the target locus in the genome. Coupling an ssODN donor with a CRISPR-Cas9-mediated DSB is one of the most streamlined approaches to introduce small changes. However, in many systems, this approach is inefficient and introduces imprecise repair at the genetic junctions. We herein report a technology that uses spatiotemporal localization of an ssODN with CRISPR-Cas9 to improve gene alteration. We show that by fusing an ssODN template to the trans-activating RNA (tracrRNA), we recover precise genetic alterations, with increased integration and precision in

Indexed as

CRISPR-Cas SystemsGene EditingDNADNA Breaks, Double-StrandedHumansRNADNARNA

Identifiers

PMID34935462
PMCPMC8892967
OpenAlexW4200075581

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.