Evidence map›Paper›PMID 23091025›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome.

Daniel W Meechan, Eric S Tucker, Thomas M Maynard, Anthony-Samuel LaMantia

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. Review
  8. Review
  9. Atypical cortical networks in children at high-genetic risk of psychiatric and neurodevelopmental disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
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  18. Review
  19. Foxg1 Regulates the Postnatal Development of Cortical Interneurons.Cerebral cortex (New York, N.Y. : 1991) · 2019
    Article
  20. Dissociable Disruptions in Thalamic and Hippocampal Resting-State Functional Connectivity in Youth with 22q11.2 Deletions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Daniel W MeechanDepartment of Pharmacology and Physiology, George Washington University, Washington, DC 20037, USA.
Eric S Tucker
Thomas M Maynard
Anthony-Samuel LaMantia
George Washington University · USWest Virginia University · US

Funding

Regulation of 22q11 Genes in Embryonic and Adult ForebrainR01HD042182 · NICHD · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI ANTHONY S LAMANTIA · 2003 to 2026
$8.6M
Roles of Growth Factor Signaling in Neural RegenerationR01NS031768 · NINDS · WASHINGTON UNIVERSITY · PI SNIDER, WILLIAM D · 1993 to 2016
$6.7M
Acquisition of Zeiss 710 Confocal Laser Scanning MicroscopeS10RR025565 · NCRR · GEORGE WASHINGTON UNIVERSITY · PI POPRATILOFF, ANASTAS · 2009 to 2009
$500k
NCRR NIH HHS S10 RR025565NCRR NIH HHS S10RR025565NICHD NIH HHS R01 HD042182NINDS NIH HHS NS031768NINDS NIH HHS R01 NS031768PHS HHS 64065Wellcome Trust 042182
6 · The paper itself

Abstract

Interneurons are thought to be a primary pathogenic target for several behavioral disorders that arise during development, including schizophrenia and autism. It is not known, however, whether genetic lesions associated with these diseases disrupt established molecular mechanisms of interneuron development. We found that diminished 22q11.2 gene dosage-the primary genetic lesion in 22q11.2 deletion syndrome (22q11.2 DS)-specifically compromises the distribution of early-generated parvalbumin-expressing interneurons in the Large Deletion (LgDel) 22q11.2DS mouse model. This change reflects cell-autonomous disruption of interneuron migration caused by altered expression of the cytokine C-X-C chemokine receptor type 4 (Cxcr4), an established regulator of this process. Cxcr4 is specifically reduced in LgDel migrating interneurons, and genetic analysis confirms that diminished Cxcr4 alters interneuron migration in LgDel mice. Thus, diminished 22q11.2 gene dosage disrupts cortical circuit development by modifying a critical molecular signaling pathway via Cxcr4 that regulates cortical interneuron migration and placement.

Indexed as

AnimalsCell MovementCerebral CortexDiGeorge SyndromeHeterozygoteInterneuronsMiceMice, Inbred C57BLMutationParvalbuminsReceptors, CXCR4CXCR4 protein, mouseParvalbuminsReceptors, CXCR4

Identifiers

PMID23091025
PMCPMC3494945
OpenAlexW2049645812

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.