Evidence map›Paper›PMID 29065506›Full record

ArticleCells2017

Expression Profiling of Differentiating Emerin-Null Myogenic Progenitor Identifies Molecular Pathways Implicated in Their Impaired Differentiation.

Ashvin Iyer, Adam J Koch, James M Holaska

Open access · goldAbstract read
In one paragraph

Article in Cells, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. The role of inner nuclear membrane protein emerin in myogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  7. Article
  8. Article
  9. The Role of Emerin in Cancer Progression and Metastasis.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. RareFrontiers in cell and developmental biology · 2019
    Article
  14. 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

3 authors at 3 institutions in 1 country.

Ashvin IyerDepartment of Pharmaceutical Sciences, University of the Sciences, Philadelphia, PA 19104, USA. aiyer@mail.usciences.edu.
Adam J KochCommittee on Genetics, Genomics and Systems Biology, University of Chicago, Chicago, IL 60637, USA. ajkoch@ucsd.edu.
James M HolaskaDepartment of Biomedical Sciences, Rm 534, Cooper Medical School of Rowan University, 401 South Broadway St., Camden, NJ 08028, USA. holaska@rowan.edu.
Cooper Medical School of Rowan University · USUniversity of Chicago · USUniversity of the Sciences · US

Funding

MULTIDISCIPLINARY CARDIAC SCIENCEST32HL007381 · NHLBI · UNIVERSITY OF CHICAGO · PI JEANNE M DECARA, Yoav Gilad · 1985 to 2026
$12.5M
Emerin regulation of myogenic differentiation: implications for muscle diseaseR15AR069935 · NIAMS · UNIVERSITY OF THE SCIENCES PHILADELPHIA · PI JAMES Michael HOLASKA · 2016 to 2026
$2.0M
NHLBI NIH HHS T32 HL007381NIAMS NIH HHS R15 AR069935
6 · The paper itself

Abstract

Mutations in the gene encoding emerin cause Emery-Dreifuss muscular dystrophy (EDMD), a disorder causing progressive skeletal muscle wasting, irregular heart rhythms and contractures of major tendons. RNA sequencing was performed on differentiating wildtype and emerin-null myogenic progenitors to identify molecular pathways implicated in EDMD, 340 genes were uniquely differentially expressed during the transition from day 0 to day 1 in wildtype cells. 1605 genes were uniquely expressed in emerin-null cells; 1706 genes were shared among both wildtype and emerin-null cells. One thousand and forty-seven transcripts showed differential expression during the transition from day 1 to day 2. Four hundred and thirty-one transcripts showed altered expression in both wildtype and emerin-null cells. Two hundred and ninety-five transcripts were differentially expressed only in emerin-null cells and 321 transcripts were differentially expressed only in wildtype cells. DAVID, STRING and Ingenuity Pathway Analysis identified pathways implicated in impaired emerin-null differentiation, including cell signaling, cell cycle checkpoints, integrin signaling, YAP/TAZ signaling, stem cell differentiation, and multiple muscle development and myogenic differentiation pathways. Functional enrichment analysis showed biological functions associated with the growth of muscle tissue and myogenesis of skeletal muscle were inhibited. The large number of differentially expressed transcripts upon differentiation induction suggests emerin functions during transcriptional reprograming of progenitors to committed myoblasts.

Indexed as

emerinEmery-Dreifuss muscular dystrophylaminmyogenic differentiation

Identifiers

PMID29065506
PMCPMC5755497
OpenAlexW2766996314

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.