Evidence map›Paper›PMID 23637330›Full record

ArticleDevelopment (Cambridge, England)2013

ASCL1 reprograms mouse Muller glia into neurogenic retinal progenitors.

Julia Pollak, Matthew S Wilken, Yumi Ueki, Kristen E Cox, Jane M Sullivan, Russell J Taylor, Edward M Levine, Thomas A Reh

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed
9.3field-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

148 citing papers in PubMed, 252 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Mesenchymal-derived neural progenitors underlie localbioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. eLife · 2026
    Article
  9. Article
  10. Regulation of the lncRNANAR molecular medicine · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Stimulating the regenerative capacity of the human retina with proneural transcription factors in 3D cultures.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Age-dependent regenerative mechanisms in the brain.Biochemical Society transactions · 2024
    Review

88 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

8 authors at 2 institutions in 1 country.

Julia PollakDepartment of Biological Structure, University of Washington, Seattle, WA 98195, USA.
Matthew S Wilken
Yumi Ueki
Kristen E Cox
Jane M Sullivan
Russell J Taylor
Edward M Levine
Thomas A Reh
University of Washington · USUniversity of Utah · US

Funding

Vision Research CoreP30EY001730 · NEI · UNIVERSITY OF WASHINGTON · PI MAUREEN E NEITZ · 1985 to 2026
$23.5M
University of Utah, Core Vision Research GrantP30EY014800 · NEI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI PAUL STEVEN BERNSTEIN · 2005 to 2026
$14.6M
Vsx2 Dependent Regulation of Retinal Progenitor Cell PropertiesR01EY013760 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LEVINE, EDWARD M · 2003 to 2024
$6.9M
Supplement to EY021482 to carry out a screen for retinal regeneration using CRISPR-Cas9 gene activation.R01EY021482 · NEI · UNIVERSITY OF WASHINGTON · PI THOMAS A REH · 2011 to 2026
$6.3M
INTERDISCIPLINARY TRAINING IN DEVELOPMENTAL BIOLOGYT32HD007183 · NICHD · UNIVERSITY OF WASHINGTON · PI RAIBLE, DAVID W · 1985 to 2015
$5.7M
NEI NIH HHS 1R01EY021482NEI NIH HHS P30 EY001730NEI NIH HHS P30 EY014800NEI NIH HHS P30EY01730NEI NIH HHS R01 EY013760NEI NIH HHS R01-EY013760NEI NIH HHS R01 EY021482NICHD NIH HHS T32 HD007183NICHD NIH HHS T32HD007183
6 · The paper itself

Abstract

Non-mammalian vertebrates have a robust ability to regenerate injured retinal neurons from Müller glia (MG) that activate the gene encoding the proneural factor Achaete-scute homolog 1 (Ascl1; also known as Mash1 in mammals) and de-differentiate into progenitor cells. By contrast, mammalian MG have a limited regenerative response and fail to upregulate Ascl1 after injury. To test whether ASCL1 could restore neurogenic potential to mammalian MG, we overexpressed ASCL1 in dissociated mouse MG cultures and intact retinal explants. ASCL1-infected MG upregulated retinal progenitor-specific genes and downregulated glial genes. Furthermore, ASCL1 remodeled the chromatin at its targets from a repressive to an active configuration. MG-derived progenitors differentiated into cells that exhibited neuronal morphologies, expressed retinal subtype-specific neuronal markers and displayed neuron-like physiological responses. These results indicate that a single transcription factor, ASCL1, can induce a neurogenic state in mature MG.

Indexed as

RegenerationAnimalsBasic Helix-Loop-Helix ProteinsBiomarkersCell ProliferationCells, CulturedCellular ReprogrammingChromatin Assembly and DisassemblyCloning, MolecularEpidermal Growth FactorGene Expression RegulationHEK293 CellsHistonesHumansIn Vitro TechniquesLentivirusAscl1 protein, mouseBasic Helix-Loop-Helix ProteinsBiomarkersEpidermal Growth FactorHistonesLuminescent ProteinsRed Fluorescent ProteinGliaMüllerNeurogenesisRegenerationReprogrammingRetina

Identifiers

PMID23637330
PMCPMC3666387
OpenAlexW2138427488

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.