Evidence map›Paper›PMID 21957244›Full record

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

Activation of postnatal neural stem cells requires nuclear receptor TLX.

Wenze Niu, Yuhua Zou, Chengcheng Shen, Chun-Li Zhang

Open access · bronzeAbstract readComparative Study
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 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

54 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
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  3. Therapeutic modulation of neurogenesis to improve hippocampal plasticity and cognition in aging and Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
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  9. Oleic acid is an endogenous ligand of TLX/NR2E1 that triggers hippocampal neurogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

4 authors at 1 institution in 1 country.

Wenze NiuDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Yuhua Zou
Chengcheng Shen
Chun-Li Zhang
The University of Texas Southwestern Medical Center · US

Funding

Neurogenesis de novo in the adult central nervous systemDP2OD006484 · OD · UT SOUTHWESTERN MEDICAL CENTER · PI ZHANG, CHUN-LI · 2009 to 2009
$2.4M
Transcriptional Control of Adult Neural Stem CellsR01NS070981 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI ZHANG, CHUN-LI · 2011 to 2015
$1.7M
NIH HHS 1DP2OD006484NIH HHS DP2 OD006484NINDS NIH HHS R01 NS070981NINDS NIH HHS R01NS070981
6 · The paper itself

Abstract

Neural stem cells (NSCs) continually produce new neurons in postnatal brains. However, the majority of these cells stay in a nondividing, inactive state. The molecular mechanism that is required for these cells to enter proliferation still remains largely unknown. Here, we show that nuclear receptor TLX (NR2E1) controls the activation status of postnatal NSCs in mice. Lineage tracing indicates that TLX-expressing cells give rise to both activated and inactive postnatal NSCs. Surprisingly, loss of TLX function does not result in spontaneous glial differentiation, but rather leads to a precipitous age-dependent increase of inactive cells with marker expression and radial morphology for NSCs. These inactive cells are mispositioned throughout the granular cell layer of the dentate gyrus during development and can proliferate again after reintroduction of ectopic TLX. RNA-seq analysis of sorted NSCs revealed a TLX-dependent global expression signature, which includes the p53 signaling pathway. TLX regulates p21 expression in a p53-dependent manner, and acute removal of p53 can rescue the proliferation defect of TLX-null NSCs in culture. Together, these findings suggest that TLX acts as an essential regulator that ensures the proliferative ability of postnatal NSCs by controlling their activation through genetic interaction with p53 and other signaling pathways.

Indexed as

AnimalsAnimals, NewbornCell ProliferationCells, CulturedHEK293 CellsHumansMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMice, TransgenicNeural Stem CellsNeurogenesisOrphan Nuclear ReceptorsReceptors, Cytoplasmic and NuclearSignal TransductionNR2E1 protein, humanOrphan Nuclear ReceptorsReceptors, Cytoplasmic and Nuclear

Identifiers

PMID21957244
PMCPMC3192402
OpenAlexW2030212579

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.