Evidence map›Paper›PMID 16648472›Full record

ArticleMolecular and cellular biology2006

Cortical thinning and hydrocephalus in mice lacking the immunoglobulin superfamily member CDO.

Wei Zhang, Min-Jeong Yi, Xiaoping Chen, Francesca Cole, Robert S Krauss, Jong-Sun Kang

Open access · greenAbstract readComparative Study
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  7. High-efficiency transduction of spinal cord motor neurons by intrauterine delivery of integration-deficient lentiviral vectors.Journal of controlled release : official journal of the Controlled Release Society · 2018
    Article
  8. Cdon deficiency causes cardiac remodeling through hyperactivation of WNT/β-catenin signaling.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Article
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  12. Fingerprint changes in CSF composition associated with different aetiologies in human neonatal hydrocephalus: inflammatory cytokines.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2014
    Article
  13. Article
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  20. Cdo promotes neuronal differentiation via activation of the p38 mitogen-activated protein kinase pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009
    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

6 authors at 1 institution in 1 country.

Wei ZhangBrookdale Department of Molecular, Cell, and Developmental Biology, Box 1020, Mount Sinai School of Medicine, New York, New York 10029, USA.
Min-Jeong Yi
Xiaoping Chen
Francesca Cole
Robert S Krauss
Jong-Sun Kang
Icahn School of Medicine at Mount Sinai · US

Funding

THE ROLE OF CDO IN MYOGENIC DIFFERENTIATIONR01AR046207 · NIAMS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI KRAUSS, ROBERT S. · 2000 to 2015
$5.1M
Mice That Lack CDO: A Model for Mild HoloprosencephalyR21DE015162 · NIDCR · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI KRAUSS, ROBERT S. · 2003 to 2004
$339k
NIAMS NIH HHS AR46207NIAMS NIH HHS R01 AR046207NIDCR NIH HHS DE15162NIDCR NIH HHS R21 DE015162
6 · The paper itself

Abstract

CDO is a cell surface immunoglobulin superfamily member that positively regulates myogenic differentiation in vitro and in vivo and signals to posttranslationally activate myogenic basic helix-loop-helix (bHLH) transcription factors. The Cdo gene is also expressed in the dorsal aspect and midline structures of the developing central nervous system, and mice lacking CDO on the C57BL/6 background display holoprosencephaly with approximately 80% penetrance, resulting in perinatal lethality. We report here that a fraction of Cdo-/- mice from this background have additional defects in brain development, including hydrocephalus and cortical thinning. Primary neural progenitor cultures from E14.5 Cdo-/- mutants display reduced proliferation, which may underlie the thinning. The cortical preplate and cortices of mutant animals also show reduced staining for beta-tubulin III, indicating defective neuronal differentiation. CDO levels are strongly increased in cultured C17.2 neuronal precursor cells stimulated to differentiate; modulation of CDO levels in these cells by overexpression or interfering RNA approaches enhances or diminishes differentiation, respectively. Cotransfection of CDO enhances the activity of the neurogenic bHLH factor, neurogenin1, in reporter assays and enhances heterodimerization of neurogenin1 and E47. These results indicate that CDO promotes neuronal differentiation and support the hypothesis that CDO coordinates differentiation of multiple cell lineages by regulating the activity of tissue-specific bHLH factors.

Indexed as

AnimalsApoptosisBasic Helix-Loop-Helix Proteinsbeta-GalactosidaseBlotting, WesternCell Adhesion MoleculesCell Culture TechniquesCell DifferentiationCell LineCell ProliferationCells, CulturedCerebral CortexCrosses, GeneticDimerizationFemaleGenes, ReporterBasic Helix-Loop-Helix Proteinsbeta-GalactosidaseBhlhe40 protein, mouseCdon protein, mouseCell Adhesion MoleculesHomeodomain ProteinsImmunoglobulinsTubulin

Identifiers

PMID16648472
PMCPMC1489002
OpenAlexW2138775922

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.