Evidence map›Paper›PMID 32988972›Full record

ArticleDisease models & mechanisms2020

A novel mouse model of Duchenne muscular dystrophy carrying a multi-exonic

Tatianna Wai Ying Wong, Abdalla Ahmed, Grace Yang, Eleonora Maino, Sydney Steiman, Elzbieta Hyatt, Parry Chan, Kyle Lindsay, Nicole Wong, Diane Golebiowski and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 26 citations in OpenAlex.

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  11. FoxP1 Represses MEF2A in Striated Muscle.Molecular and cellular biology · 2024
    Article
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  19. AInternational journal of molecular sciences · 2021
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 2 countries.

Tatianna Wai Ying WongProgram in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.
Abdalla AhmedProgram in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.
Grace YangProgram in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.
Eleonora MainoProgram in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.
Sydney SteimanProgram in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.
Elzbieta HyattProgram in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.
Parry ChanProgram in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.
Kyle LindsayProgram in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.
Nicole WongProgram in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.
Diane GolebiowskiSolid Biosciences, Cambridge, MA 02142, USA.
Joel SchneiderSolid Biosciences, Cambridge, MA 02142, USA.
Paul Delgado-OlguínProgram in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.ORCID 0000-0002-5355-247X
Evgueni A IvakineProgram in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.ORCID 0000-0003-2132-4699
Ronald D CohnProgram in Genetics and Genome Biology, The Hospital for Sick Children Research Institute, Toronto, ON M5G 0A4, Canada.ORCID 0000-0002-2673-696X
Hospital for Sick Children · CAUniversity of Toronto · CASolidus Biosciences (United States) · US

Funding

CIHR 6210100686
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a life-threatening neuromuscular disease caused by the lack of dystrophin, resulting in progressive muscle wasting and locomotor dysfunctions. By adulthood, almost all patients also develop cardiomyopathy, which is the primary cause of death in DMD. Although there has been extensive effort in creating animal models to study treatment strategies for DMD, most fail to recapitulate the complete skeletal and cardiac disease manifestations that are presented in affected patients. Here, we generated a mouse model mirroring a patient deletion mutation of exons 52-54 (

Indexed as

Gene DeletionAnimalsBase SequenceCardiomegalyCardiomyopathiesCRISPR-Cas SystemsDisease Models, AnimalDystroglycansDystrophinExonsFemaleMice, Inbred C57BLMice, TransgenicMuscle, SkeletalMuscle StrengthMuscular Dystrophy, DuchenneDystroglycansDystrophinCardiomyopathyDeletion mutationDMDMouse modelMuscular dystrophy

Identifiers

PMID32988972
PMCPMC7522028
OpenAlexW3087452454

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.