Evidence map›Paper›PMID 21689730›Full record

ArticleNeuroscience2011

Dcdc2 knockout mice display exacerbated developmental disruptions following knockdown of doublecortin.

Y Wang, X Yin, G Rosen, L Gabel, S M Guadiana, M R Sarkisian, A M Galaburda, J J Loturco

Abstract read
In one paragraph

Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Animal models of developmental dyslexia.Frontiers in neuroscience · 2022
    Review
  5. Renal Ciliopathies: Sorting Out Therapeutic Approaches for Nephronophthisis.Frontiers in cell and developmental biology · 2021
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Neural Noise Hypothesis of Developmental Dyslexia.Trends in cognitive sciences · 2017
    Review
  13. Article
  14. Review
  15. Review
  16. Knockdown of Dyslexia-Gene Dcdc2 Interferes with Speech Sound Discrimination in Continuous Streams.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  17. Article
  18. Review
  19. Article
  20. 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

8 authors at 4 institutions in 1 country.

Y WangDepartment of Physiology and Neurobiology, University of Connecticut, Storrs, CT 06269, USA.
X Yin
G Rosen
L Gabel
S M Guadiana
M R Sarkisian
A M Galaburda
J J Loturco
University of Connecticut · USBeth Israel Deaconess Medical Center · USUniversity of Florida · USLafayette College · US

Funding

PROJ 3: NEUROBEHAVIOR: BEHAVIOTAL CONSEQUENCES OF EMBRYONIC DISRUPTIONP01HD057853 · NICHD · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LOTURCO, JOSEPH J · 2009 to 2014
$5.3M
MOLECULAR REGULATION OF NEOCORTICAL NEUROGENESISR01MH056524 · NIMH · UNIVERSITY OF CONNECTICUT STORRS · PI LOTURCO, JOSEPH J · 2003 to 2012
$3.3M
DYSLEXIA SUSCEPTIBILITY GENES AND MECHANISMS OF NEURONAL DEVELOPMENTR01HD055655 · NICHD · UNIVERSITY OF CONNECTICUT STORRS · PI LOTURCO, JOSEPH J · 2008 to 2012
$1.6M
NICHD NIH HHS HD055655NICHD NIH HHS HD057853NICHD NIH HHS P01 HD057853NICHD NIH HHS R01 HD055655NIMH NIH HHS R01 MH056524
6 · The paper itself

Abstract

The dyslexia-associated gene DCDC2 is a member of the DCX family of genes known to play roles in neurogenesis, neuronal migration, and differentiation. Here we report the first phenotypic analysis of a Dcdc2 knockout mouse. Comparisons between Dcdc2 knockout mice and wild-type (wt) littermates revealed no significant differences in neuronal migration, neocortical lamination, neuronal cilliogenesis or dendritic differentiation. Considering previous studies showing genetic interactions and potential functional redundancy among members of the DCX family, we tested whether decreasing Dcx expression by RNAi would differentially impair neurodevelopment in Dcdc2 knockouts and wild-type mice. Consistent with this hypothesis, we found that deficits in neuronal migration, and dendritic growth caused by RNAi of Dcx were more severe in Dcdc2 knockouts than in wild-type mice with the same transfection. These results indicate that Dcdc2 is not required for neurogenesis, neuronal migration or differentiation in mice, but may have partial functional redundancy with Dcx.

Indexed as

AnimalsBehavior, AnimalCell MovementDendritesDoublecortin Domain ProteinsDoublecortin ProteinMiceMice, KnockoutMicrotubule-Associated ProteinsNeocortexNeurogenesisNeuronsNeuropeptidesDcx protein, mouseDoublecortin Domain ProteinsDoublecortin ProteinMicrotubule-Associated ProteinsNeuropeptides

Identifiers

PMID21689730
PMCPMC3170724
OpenAlexW2092904511

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.