Evidence map›Paper›PMID 15078815›Full record

ArticleGenes & development2004

Conversion of myoblasts to physiologically active neuronal phenotype.

Yumi Watanabe, Sei Kameoka, Vidya Gopalakrishnan, Kenneth D Aldape, Zhizhong Z Pan, Frederick F Lang, Sadhan Majumder

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
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  8. miR-124-3p is a chronic regulator of gene expression after brain injury.Cellular and molecular life sciences : CMLS · 2018
    Article
  9. Polypyrimidine tract-binding protein blocks miRNA-124 biogenesis to enforce its neuronal-specific expression in the mouse.Proceedings of the National Academy of Sciences of the United States of America · 2018
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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

7 authors at 2 institutions in 2 countries.

Yumi WatanabeDepartment of Molecular Genetics, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
Sei Kameoka
Vidya Gopalakrishnan
Kenneth D Aldape
Zhizhong Z Pan
Frederick F Lang
Sadhan Majumder
The University of Texas MD Anderson Cancer Center · USLaboratory of Molecular Genetics · PL

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TRANSCRIPTION FACTOR REST/NRSF IN MEDULLOBLASTOMAR01CA081255 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MAJUMDER, SADHAN · 1999 to 2010
$2.1M
Opioid Receptors in the Mechanisms of Opioid ToleranceR01DA014524 · NIDA · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI PAN, ZHIZHONG Z · 2001 to 2005
$1.3M
NCI NIH HHS CA 16672NCI NIH HHS CA 81255NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA081255NIDA NIH HHS R01 DA014524
6 · The paper itself

Abstract

Repressor element 1 (RE1)-silencing transcription factor (REST)/neuron-restrictive silencer factor (NRSF) can repress several terminal neuronal differentiation genes by binding to a specific DNA sequence (RE1/neuron-restrictive silencer element [NRSE]) present in their regulatory regions. REST-VP16 binds to the same RE1/NRSE, but activates these REST/NRSF target genes. However, it is unclear whether REST-VP16 expression is sufficient to cause formation of functional neurons either from neural stem cells or from heterologous stem cells. Here we show that the expression of REST-VP16 in myoblasts grown under muscle differentiation conditions blocked entry into the muscle differentiation pathway, countered endogenous REST/NRSF-dependent repression, activated the REST/NRSF target genes, and, surprisingly, activated other neuronal differentiation genes and converted the myoblasts to a physiologically active neuronal phenotype. Furthermore, in vitro differentiated neurons produced by REST-VP16-expressing myoblasts, when injected into mouse brain, survived, incorporated into the normal brain, and did not form tumors. This is the first instance in which myoblasts were converted to a neuronal phenotype. Our results suggest that direct activation of REST/NRSF target genes with a single transgene, REST-VP16, is sufficient to activate other terminal neuronal differentiation genes and to override the muscle differentiation pathways, and they suggest that this approach provides an efficient way of triggering neuronal differentiation in myoblasts and possibly other stem cells.

Indexed as

AnimalsCell DifferentiationMiceMuscle CellsMyoblastsNeuronsRE1-Silencing Transcription FactorRepressor ProteinsTranscription FactorsRE1-Silencing Transcription FactorRepressor ProteinsTranscription Factors

Identifiers

PMID15078815
PMCPMC395848
OpenAlexW2096245934

What OpenQuestion holds

Textmetadata
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.