Evidence map›Paper›PMID 29618840›Full record

ArticleScientific reports2018

SMAD6 overexpression leads to accelerated myogenic differentiation of LMNA mutated cells.

Alexandre Janin, Delphine Bauer, Francesca Ratti, Camille Valla, Anne Bertrand, Emilie Christin, Emilie Chopin, Nathalie Streichenberger, Gisèle Bonne, Vincent Gache and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. The Influence of theAnimals : an open access journal from MDPI · 2026
    Article
  2. Review
  3. Consequences ofCells · 2020
    Article
  4. Review
  5. [Clinical and genetic features of limb-girdle muscular dystrophy type 1B: a case report].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018
    Article
  6. 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 4 institutions in 2 countries.

Alexandre JaninUniversity of Lyon, University of Lyon1 Claude Bernard Lyon1, Institut NeuroMyoGene, CNRS UMR5310, INSERM U1217, Lyon, France. alexandre.janin01@chu-lyon.fr.ORCID 0000-0003-3571-003X
Delphine BauerUniversity of Lyon, University of Lyon1 Claude Bernard Lyon1, Institut NeuroMyoGene, CNRS UMR5310, INSERM U1217, Lyon, France.
Francesca RattiUniversity of Lyon, University of Lyon1 Claude Bernard Lyon1, Institut NeuroMyoGene, CNRS UMR5310, INSERM U1217, Lyon, France.
Camille VallaUniversity of Lyon, University of Lyon1 Claude Bernard Lyon1, Institut NeuroMyoGene, CNRS UMR5310, INSERM U1217, Lyon, France.
Anne BertrandSorbonne Université, INSERM UMRS_974, Center of Research in Myology, 75013, Paris, France.
Emilie ChristinUniversity of Lyon, University of Lyon1 Claude Bernard Lyon1, Institut NeuroMyoGene, CNRS UMR5310, INSERM U1217, Lyon, France.
Emilie ChopinCentre de Biotechnologie Cellulaire, Centre de Biologie et Pathologie Est, Hospices Civils de Lyon, F-69677, Bron, France.
Nathalie StreichenbergerUniversity of Lyon, University of Lyon1 Claude Bernard Lyon1, Institut NeuroMyoGene, CNRS UMR5310, INSERM U1217, Lyon, France.
Gisèle BonneSorbonne Université, INSERM UMRS_974, Center of Research in Myology, 75013, Paris, France.ORCID 0000-0002-2516-3258
Vincent GacheUniversity of Lyon, University of Lyon1 Claude Bernard Lyon1, Institut NeuroMyoGene, CNRS UMR5310, INSERM U1217, Lyon, France.
Tatiana CohenResearch Center for Genetic Medicine, Children's National Medical Center, 111 Michigan Avenue NW, Washington, DC, 20010, USA.
Alexandre MéjatUniversity of Lyon, University of Lyon1 Claude Bernard Lyon1, Institut NeuroMyoGene, CNRS UMR5310, INSERM U1217, Lyon, France. alexandre.mejat@ens-lyon.fr.
Université Claude Bernard Lyon 1 · FRInserm · FRChildren's National · USHospices Civils de Lyon · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

LMNA gene encodes lamins A and C, two major components of the nuclear lamina, a network of intermediate filaments underlying the inner nuclear membrane. Most of LMNA mutations are associated with cardiac and/or skeletal muscles defects. Muscle laminopathies include Emery-Dreifuss Muscular Dystrophy, Limb-Girdle Muscular Dystrophy 1B, LMNA-related Congenital Muscular Dystrophy and Dilated Cardiomyopathy with conduction defects. To identify potential alterations in signaling pathways regulating muscle differentiation in LMNA-mutated myoblasts, we used a previously described model of conditionally immortalized murine myoblasts: H-2K cell lines. Comparing gene expression profiles in wild-type and Lmna

Indexed as

Cell DifferentiationMutationAdultAnimalsBone Morphogenetic Protein 4Case-Control StudiesHumansLamin Type AMaleMiceMice, KnockoutMuscle DevelopmentMuscular Dystrophy, Emery-DreifussMyoblastsSmad6 ProteinBMP4 protein, humanBmp4 protein, mouseBone Morphogenetic Protein 4Lamin Type ALMNA protein, humanLmna protein, mouseSmad6 ProteinSMAD6 protein, humanSmad6 protein, mouse

Identifiers

PMID29618840
PMCPMC5884786
OpenAlexW2795771082

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.