Evidence map›Paper›PMID 24968361›Full record

ArticleDevelopmental biology2014

Arx together with FoxA2, regulates Shh floor plate expression.

Ginam Cho, Youngshin Lim, Il-Taeg Cho, Jacqueline C Simonet, Jeffrey A Golden

Abstract read
In one paragraph

Article in Developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
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  4. Mirk/Dyrk1B controls ventral spinal cord development via Shh pathway.Cellular and molecular life sciences : CMLS · 2024
    Article
  5. Article
  6. Persistence of FoxJ1Cellular and molecular life sciences : CMLS · 2023
    Article
  7. Review
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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

5 authors at 2 institutions in 1 country.

Ginam ChoDepartment of Pathology, Brigham and Women׳s Hospital, Harvard Medical School, USA; Department of Pathology and Laboratory Medicine, Children׳s Hospital of Philadelphia, USA.
Youngshin LimDepartment of Pathology, Brigham and Women׳s Hospital, Harvard Medical School, USA.
Il-Taeg ChoDepartment of Pathology, Brigham and Women׳s Hospital, Harvard Medical School, USA.
Jacqueline C SimonetCell and Molecular Biology Graduate Group, Perelman School of Medicine, University of Pennsylvania, USA.
Jeffrey A GoldenDepartment of Pathology, Brigham and Women׳s Hospital, Harvard Medical School, USA; Department of Pathology and Laboratory Medicine, Children׳s Hospital of Philadelphia, USA. Electronic address: jagolden@partners.org.
Brigham and Women's Hospital · USUniversity of Pennsylvania · US

Funding

The Role of ARX in Normal and Abnormal Brain DevelopmentR01NS046616 · NINDS · CHILDREN'S HOSP OF PHILADELPHIA · PI GOLDEN, JEFFREY A · 2005 to 2013
$4.1M
NINDS NIH HHS NS46616NINDS NIH HHS R01 NS046616
6 · The paper itself

Abstract

Mutations in the Aristaless related homeodomain transcription factor (ARX) are associated with a diverse set of X-linked mental retardation and epilepsy syndromes in humans. Although most studies have been focused on its function in the forebrain, ARX is also expressed in other regions of the developing nervous system including the floor plate (FP) of the spinal cord where its function is incompletely understood. To investigate the role of Arx in the FP, we performed gain-of-function studies in the chick using in ovo electroporation, and loss-of-function studies in Arx-deficient mice. We have found that Arx, in conjunction with FoxA2, directly induces Sonic hedgehog (Shh) expression through binding to a Shh floor plate enhancer (SFPE2). We also observed that FoxA2 induces Arx through its transcriptional activation domain whereas Nkx2.2, induced by Shh, abolishes this induction. Our data support a feedback loop model for Arx function; through interactions with FoxA2, Arx positively regulates Shh expression in the FP, and Shh signaling in turn activates Nkx2.2, which suppresses Arx expression. Furthermore, our data are evidence that Arx plays a role as a context dependent transcriptional activator, rather than a primary inducer of Shh expression, potentially explaining how mutations in ARX are associated with diverse, and often subtle, defects.

Indexed as

AnimalsChick EmbryoEpilepsyGene Expression Regulation, DevelopmentalHedgehog ProteinsHepatocyte Nuclear Factor 3-betaHomeobox Protein Nkx-2.2Homeodomain ProteinsMiceMice, Inbred C57BLMice, KnockoutMutationNeural TubeNuclear ProteinsSpinal CordTranscription FactorsARX protein, mouseFoxa2 protein, mouseHedgehog ProteinsHepatocyte Nuclear Factor 3-betaHomeobox Protein Nkx-2.2Homeodomain Proteinsnkx2.2b protein, zebrafishNKX2-2 protein, humanNkx2-2 protein, mouseNuclear ProteinsShh protein, mouseTranscription FactorsZebrafish ProteinsArxDevelopmentFloor plateFoxA2Neural tubeNkx2.2ShhSpinal cord

Identifiers

PMID24968361
PMCPMC4681535
OpenAlexW2055856797

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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.