Evidence map›Paper›PMID 21248112›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Gdf11 facilitates temporal progression of neurogenesis in the developing spinal cord.

Yingtang Shi, Jeh-Ping Liu

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

39 citing papers in PubMed, 70 citations in OpenAlex.

  1. bioRxiv : the preprint server for biology · 2025
    Article
  2. A spatially organizedScience advances · 2025
    Article
  3. Article
  4. Article
  5. GDF11: An emerging therapeutic target for liver diseases and fibrosis.Journal of cellular and molecular medicine · 2024
    Review
  6. Article
  7. Temporal regulation of neural diversity in Drosophila and vertebrates.Seminars in cell & developmental biology · 2023
    Review
  8. Article
  9. Article
  10. Heterozygous loss-of-function variants significantly expand the phenotypes associated with loss of GDF11.Genetics in medicine : official journal of the American College of Medical Genetics · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Anti-Aging Effects of GDF11 on Skin.International journal of molecular sciences · 2020
    Review
  18. Review
  19. Functional Versatility of the CDK Inhibitor p57Frontiers in cell and developmental biology · 2020
    Review
  20. 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

2 authors at 1 institution in 1 country.

Yingtang ShiDepartment of Neuroscience, University of Virginia School of Medicine, Charlottesville, Virginia 22908, USA.
Jeh-Ping Liu
University of Virginia · US

Funding

Control of Hox gene expression and neuronal identityR01NS045933 · NINDS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI LIU, JEH-PING · 2003 to 2007
$1.6M
NINDS NIH HHS R01 NS045933
6 · The paper itself

Abstract

Various types of neurons and glia are generated following a precise spatial and temporal order during neurogenesis. The mechanisms that control this sequential generation of neuronal and glial cell types from the same progenitor population are not well understood. Growth differentiation factor 11 (Gdf11) belongs to the TGF-β family of proteins and is expressed transiently in newly born neurons adjacent to the progenitor domain in the developing spinal cord. We examined the phenotypes of Gdf11(-/-) mouse embryos and found that without Gdf11, neuronal differentiation in the spinal cord progresses at a slower rate. Higher progenitor proliferation rate, along with a delay in gliogenesis, is also observed in Gdf11(-/-) spinal cord but only after the peak of Gdf11 expression, indicating that Gdf11 can cause long-lasting changes in progenitor properties. These changes can be preserved in vitro, as neurospheres derived from Gdf11(-/-) and wild-type littermates at a stage after, but not before the onset of Gdf11 expression, exhibit differences in proliferation and differentiation potential. Moreover, these changes in progenitor properties can be induced in vitro by the addition of Gdf11. We also demonstrate that the effects of Gdf11 on progenitor cells are associated with its ability to upregulate p57(Kip2) and p27(Kip1) while downregulating Pax6 expression. These results support a model in which Gdf11 secreted by newly born neurons in the developing spinal cord facilitates the temporal progression of neurogenesis by acting as a positive feedback signal on the progenitor cells to promote cell cycle exit and decrease proliferation ability, thus changing their differentiation potential.

Indexed as

AnimalsBlotting, WesternBone Morphogenetic ProteinsCell CountCell CycleCell ProliferationCyclin-Dependent Kinase Inhibitor p57Eye ProteinsGene Expression Regulation, DevelopmentalGrowth Differentiation FactorsHomeodomain ProteinsIn Situ HybridizationMiceMice, KnockoutNeurogenesisNeuronsBone Morphogenetic ProteinsCdkn1c protein, mouseCyclin-Dependent Kinase Inhibitor p57Eye ProteinsGdf11 protein, mouseGrowth Differentiation FactorsHomeodomain Proteinsp27 antigenPaired Box Transcription FactorsPax6 protein, mousePAX6 Transcription FactorProliferating Cell Nuclear AntigenRepressor Proteins

Identifiers

PMID21248112
PMCPMC4112097
OpenAlexW2047674872

What OpenQuestion holds

Textmetadata
LicenceTDM
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.