Evidence map›Paper›PMID 35270040›Full record

ArticleInternational journal of molecular sciences2022

Generation of a Dystrophin Mutant in Dog by Nuclear Transfer Using CRISPR/Cas9-Mediated Somatic Cells: A Preliminary Study.

Hyun Ju Oh, Eugene Chung, Jaehwan Kim, Min Jung Kim, Geon A Kim, Seok Hee Lee, Kihae Ra, Kidong Eom, Soojin Park, Jong-Hee Chae and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 43% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Review
  3. Dog models of human atherosclerotic cardiovascular diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2023
    Review
  4. Review
  5. 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

12 authors at 2 institutions in 1 country.

Hyun Ju OhDepartment of Theriogenology and Biotechnology, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.ORCID 0000-0002-6861-8857
Eugene ChungCenter for Genome Engineering, Institute for Basic Science, Seoul 08826, Korea.
Jaehwan KimDepartment of Veterinary Medical Imaging, College of Veterinary Medicine, Konkuk University, Seoul 5029, Korea.ORCID 0000-0002-5728-4820
Min Jung KimDepartment of Theriogenology and Biotechnology, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Geon A KimDepartment of Theriogenology and Biotechnology, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.ORCID 0000-0002-5868-1297
Seok Hee LeeDepartment of Theriogenology and Biotechnology, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Kihae RaDepartment of Theriogenology and Biotechnology, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Kidong EomDepartment of Veterinary Medical Imaging, College of Veterinary Medicine, Konkuk University, Seoul 5029, Korea.
Soojin ParkDepartment of Pediatrics, Seoul National University College of Medicine, Seoul 03080, Korea.
Jong-Hee ChaeDepartment of Pediatrics, Seoul National University College of Medicine, Seoul 03080, Korea.
Jin-Soo KimCenter for Genome Engineering, Institute for Basic Science, Seoul 08826, Korea.
Byeong Chun LeeDepartment of Theriogenology and Biotechnology, College of Veterinary Medicine, Seoul National University, Seoul 08826, Korea.
Seoul National University · KRKonkuk University · KR

Funding

Institute for Basic Science IBS-R021-D1Nature Cell #550-20200076
6 · The paper itself

Abstract

Dystrophinopathy is caused by mutations in the dystrophin gene, which lead to progressive muscle degeneration, necrosis, and finally, death. Recently, golden retrievers have been suggested as a useful animal model for studying human dystrophinopathy, but the model has limitations due to difficulty in maintaining the genetic background using conventional breeding. In this study, we successfully generated a dystrophin mutant dog using the CRISPR/Cas9 system and somatic cell nuclear transfer. The dystrophin mutant dog displayed phenotypes such as elevated serum creatine kinase, dystrophin deficiency, skeletal muscle defects, an abnormal electrocardiogram, and avoidance of ambulation. These results indicate that donor cells with CRISPR/Cas9 for a specific gene combined with the somatic cell nuclear transfer technique can efficiently produce a dystrophin mutant dog, which will help in the successful development of gene therapy drugs for dogs and humans.

Indexed as

DystrophinMuscular Dystrophy, DuchenneAnimalsCRISPR-Cas SystemsDogsGene EditingMuscle, SkeletalNuclear Transfer TechniquesDystrophinCRISPR/Cas9dogdystrophinmutantsomatic cell nuclear transfer

Identifiers

PMID35270040
PMCPMC8911381
OpenAlexW4220828622

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.