Evidence map›Paper›PMID 20610763›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Interactions of Wnt/beta-catenin signaling and sonic hedgehog regulate the neurogenesis of ventral midbrain dopamine neurons.

Mianzhi Tang, J Carlos Villaescusa, Sarah X Luo, Camilla Guitarte, Simonia Lei, Yasunori Miyamoto, Makoto M Taketo, Ernest Arenas, Eric J Huang

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
6.0field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 115 citations in OpenAlex.

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  3. Neuroprotective role of bilirubin in Parkinson's disease.Frontiers in aging neuroscience · 2026
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  9. On the Road from Phenotypic Plasticity to Stem Cell Therapy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
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  11. Frontiers in genetics · 2021
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  13. Cells · 2020
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  14. Review
  15. Loss of HIPK2 Protects Neurons from Mitochondrial Toxins by Regulating Parkin Protein Turnover.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  16. Article
  17. Article
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  19. Review
  20. Review

6 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

9 authors at 5 institutions in 3 countries.

Mianzhi TangDepartment of Pathology, University of California, San Francisco and Pathology Service, Veterans Affairs Medical Center, San Francisco, California 94121, USA.
J Carlos Villaescusa
Sarah X Luo
Camilla Guitarte
Simonia Lei
Yasunori Miyamoto
Makoto M Taketo
Ernest Arenas
Eric J Huang
San Francisco VA Medical Center · USKarolinska Institutet · SEKyoto University · JPOchanomizu University · JPUniversity of California, San Francisco · US

Funding

Signaling pathways of HIPK2 in neuronal apoptosisR01NS048393 · NINDS · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI HUANG, ERIC J · 2005 to 2009
$1.5M
Mouse models of neuroprotection in dopamine neuronsK26RR024858 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HUANG, ERIC J · 2009 to 2011
$469k
Mouse models of neuroprotection in dopamine neuronsK26OD010927 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HUANG, ERIC J · 2012 to 2013
$307k
NCRR NIH HHS K26 RR024858NCRR NIH HHS RR24858NIH HHS K26 OD010927NINDS NIH HHS NS48393NINDS NIH HHS R01 NS048393
6 · The paper itself

Abstract

Signaling mechanisms involving Wnt/beta-catenin and sonic hedgehog (Shh) are known to regulate the development of ventral midbrain (vMB) dopamine neurons. However, the interactions between these two mechanisms and how such interactions can be targeted to promote a maximal production of dopamine neurons are not fully understood. Here we show that conditional mouse mutants with region-specific activation of beta-catenin signaling in vMB using the Shh-Cre mice show a marked expansion of Sox2-, Ngn2-, and Otx2-positive progenitors but perturbs their cell cycle exit and reduces the generation of dopamine neurons. Furthermore, activation of beta-catenin in vMB also results in a progressive loss of Shh expression and Shh target genes. Such antagonistic effects between the activation of Wnt/beta-catenin and Shh can be recapitulated in vMB progenitors and in mouse embryonic stem cell cultures. Notwithstanding these antagonistic interactions, cell-type-specific activation of beta-catenin in the midline progenitors using the tyrosine hydroxylase-internal ribosomal entry site-Cre (Th-IRES-Cre) mice leads to increased dopaminergic neurogenesis. Together, these results indicate the presence of a delicate balance between Wnt/beta-catenin and Shh signaling mechanisms in the progression from progenitors to dopamine neurons. Persistent activation of beta-catenin in early progenitors perturbs their cell cycle progression and antagonizes Shh expression, whereas activation of beta-catenin in midline progenitors promotes the generation of dopamine neurons.

Indexed as

Age FactorsAnimalsAnimals, Newbornbeta CateninBromodeoxyuridineCell CountCell DifferentiationCells, CulturedDNA-Binding ProteinsDopamineEmbryo, MammalianEnzyme InhibitorsGene Expression Regulation, DevelopmentalGreen Fluorescent ProteinsHedgehog ProteinsIntercellular Signaling Peptides and Proteinsbeta CateninBromodeoxyuridineChir 99021CTNNB1 protein, mouseDNA-Binding ProteinsDopamineenhanced green fluorescent proteinEnzyme InhibitorsGreen Fluorescent ProteinsHedgehog ProteinsIntercellular Signaling Peptides and ProteinsNerve Tissue ProteinsNuiP protein, mousePyridinesPyrimidinesShh protein, mouseTyrosine 3-MonooxygenaseWnt1 ProteinWnt1 protein, mouse

Identifiers

PMID20610763
PMCPMC3578394
OpenAlexW1993209089

What OpenQuestion holds

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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.