Evidence map›Paper›PMID 38802640›Full record

ArticleMolecular neurobiology2024

Expression of Dystrophin Dp71 Splice Variants Is Temporally Regulated During Rodent Brain Development.

Mayram González-Reyes, Jorge Aragón, Alejandra Sánchez-Trujillo, Griselda Rodríguez-Martínez, Kevin Duarte, Evangelia Eleftheriou, Jean-Vianney Barnier, Delphine Naquin, Claude Thermes, José Romo-Yáñez and 4 more

Abstract read
In one paragraph

Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. The behavioural consequences of dystrophinopathy.Disease models & mechanisms · 2025
    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

14 authors.

Mayram González-ReyesDepartamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV), Mexico City, Mexico.
Jorge AragónDepartamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV), Mexico City, Mexico.
Alejandra Sánchez-TrujilloDepartamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV), Mexico City, Mexico.
Griselda Rodríguez-MartínezDepartamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV), Mexico City, Mexico.
Kevin DuarteInstitut des Neurosciences Paris Saclay, Université Paris-Saclay, CNRS, Saclay, 91400, France.
Evangelia EleftheriouInstitute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS, Gif-sur-Yvette, 91198, France.
Jean-Vianney BarnierInstitut des Neurosciences Paris Saclay, Université Paris-Saclay, CNRS, Saclay, 91400, France.
Delphine NaquinInstitute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS, Gif-sur-Yvette, 91198, France.
Claude ThermesInstitute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS, Gif-sur-Yvette, 91198, France.
José Romo-YáñezDepartamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV), Mexico City, Mexico.
Jérome E RogerInstitut des Neurosciences Paris Saclay, Université Paris-Saclay, CNRS, Saclay, 91400, France.
Alvaro RendonInstitut de la Vision, Sorbonne Université-INSERM-CNRS, 17 rue Moreau, Paris, 75012, France.
Cyrille VaillendInstitut des Neurosciences Paris Saclay, Université Paris-Saclay, CNRS, Saclay, 91400, France. cyrille.vaillend@universite-paris-saclay.fr.
Cecilia MontanezDepartamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV), Mexico City, Mexico. cecim@cinvestav.mx.

Funding

Consejo Nacional de Ciencia y Tecnología (CONACyT) CB A1-S-24868ECOS Nord supporting France-Mexico M16SO1/276330
6 · The paper itself

Abstract

Dystrophin Dp71 is the major product of the Duchenne muscular dystrophy (DMD) gene in the brain, and its loss in DMD patients and mouse models leads to cognitive impairments. Dp71 is expressed as a range of proteins generated by alternative splicing of exons 71 to 74 and 78, classified in the main Dp71d and Dp71f groups that contain specific C-terminal ends. However, it is unknown whether each isoform has a specific role in distinct cell types, brain regions, and/or stages of brain development. In the present study, we characterized the expression of Dp71 isoforms during fetal (E10.5, E15.5) and postnatal (P1, P7, P14, P21 and P60) mouse and rat brain development. We finely quantified the expression of several Dp71 transcripts by RT-PCR and cloning assays in samples from whole-brain and distinct brain structures. The following Dp71 transcripts were detected: Dp71d, Dp71d

Indexed as

BrainDystrophinGene Expression Regulation, DevelopmentalProtein IsoformsAlternative SplicingAnimalsAnimals, NewbornMaleMiceMice, Inbred C57BLRatsRNA, Messengerapo-dystrophin 1DystrophinProtein IsoformsRNA, MessengerDp71 isoformsDuchenne muscular dystrophyFetal brainHippocampus, cortex, cerebellumNanopore sequencingPostnatal brain development

Identifiers

PMID38802640
PMCPMC11584426

What OpenQuestion holds

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LicenceCC BY
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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.