Evidence map›Paper›PMID 26582133›Full record

ArticleCell2015

Jagged 1 Rescues the Duchenne Muscular Dystrophy Phenotype.

Natassia M Vieira, Ingegerd Elvers, Matthew S Alexander, Yuri B Moreira, Alal Eran, Juliana P Gomes, Jamie L Marshall, Elinor K Karlsson, Sergio Verjovski-Almeida, Kerstin Lindblad-Toh and 2 more

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

Article in Cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
9.9field-weighted citation impact, top 1% 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

91 citing papers in PubMed, 158 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Canine Model of Duchenne Muscular Dystrophy.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  6. Article
  7. Muscle-specific increased expression ofProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. NOTCH2 mutation in centronuclear myopathy: Beyond the scope.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  9. Review
  10. Article
  11. Review
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  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
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  20. Article

31 more citing papers are in PubMed but not listed here.

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 4 institutions in 4 countries.

Natassia M VieiraThe Division of Genetics and Genomics, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics and Genetics, Harvard Medical School, Boston, MA 02115, USA; Human Genome and Stem Cell Center, Biosciences Institute, University of São Paulo, São Paulo 05508-090, Brazil.
Ingegerd ElversBroad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Science for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, Box 597, 751 24, Uppsala, Sweden.
Matthew S AlexanderThe Division of Genetics and Genomics, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics and Genetics, Harvard Medical School, Boston, MA 02115, USA; The Stem Cell Program at Boston Children's Hospital, Boston, MA 02115, USA.
Yuri B MoreiraDepartamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil, 05508-000.
Alal EranDepartment of Pediatrics and Genetics, Harvard Medical School, Boston, MA 02115, USA.
Juliana P GomesHuman Genome and Stem Cell Center, Biosciences Institute, University of São Paulo, São Paulo 05508-090, Brazil.
Jamie L MarshallThe Division of Genetics and Genomics, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics and Genetics, Harvard Medical School, Boston, MA 02115, USA.
Elinor K KarlssonBroad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Program in Bioinformatics and Integrative Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Sergio Verjovski-AlmeidaDepartamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil, 05508-000; Instituto Butantan, São Paulo 05508-050, Brazil.
Kerstin Lindblad-TohBroad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Science for Life Laboratory, Department of Medical Biochemistry and Microbiology, Uppsala University, Box 597, 751 24, Uppsala, Sweden.
Louis M KunkelThe Division of Genetics and Genomics, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics and Genetics, Harvard Medical School, Boston, MA 02115, USA; The Manton Center for Orphan Disease Research at Boston Children's Hospital, Boston, MA 02115, USA. Electronic address: kunkel@enders.tch.harvard.edu.
Mayana ZatzHuman Genome and Stem Cell Center, Biosciences Institute, University of São Paulo, São Paulo 05508-090, Brazil. Electronic address: mayazatz@usp.br.
Boston Children's Hospital · USUniversidade de São Paulo · BRBroad Institute · USHarvard University · US

Funding

Modulation of Jagged1/Pitpna in DMD as a means of therapyR01AR064300 · NIAMS · BOSTON CHILDREN'S HOSPITAL · PI KUNKEL, LOUIS M · 2014 to 2023
$3.9M
NIAMS NIH HHS R01 AR064300NIAMS NIH HHS R01AR064300
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD), caused by mutations at the dystrophin gene, is the most common form of muscular dystrophy. There is no cure for DMD and current therapeutic approaches to restore dystrophin expression are only partially effective. The absence of dystrophin in muscle results in dysregulation of signaling pathways, which could be targets for disease therapy and drug discovery. Previously, we identified two exceptional Golden Retriever muscular dystrophy (GRMD) dogs that are mildly affected, have functional muscle, and normal lifespan despite the complete absence of dystrophin. Now, our data on linkage, whole-genome sequencing, and transcriptome analyses of these dogs compared to severely affected GRMD and control animals reveals that increased expression of Jagged1 gene, a known regulator of the Notch signaling pathway, is a hallmark of the mild phenotype. Functional analyses demonstrate that Jagged1 overexpression ameliorates the dystrophic phenotype, suggesting that Jagged1 may represent a target for DMD therapy in a dystrophin-independent manner. PAPERCLIP.

Indexed as

Disease Models, AnimalAnimalsCalcium-Binding ProteinsCell ProliferationDog DiseasesDogsDystrophinFemaleGenome-Wide Association StudyIntercellular Signaling Peptides and ProteinsJagged-1 ProteinMaleMembrane ProteinsMiceMuscular Dystrophy, AnimalMuscular Dystrophy, DuchenneCalcium-Binding ProteinsDystrophinIntercellular Signaling Peptides and Proteinsjag1a protein, zebrafishJAG1 protein, humanJag1 protein, mouseJagged-1 ProteinMembrane ProteinsSerrate-Jagged ProteinsZebrafish ProteinsDMDdystrophingenetic modifierJagged1muscle

Identifiers

PMID26582133
PMCPMC4668935
OpenAlexW2175838118

What OpenQuestion holds

Textmetadata
LicenceTDM
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.