Evidence map›Paper›PMID 26728762›Full record

ArticleScientific reports2016

Missense mutation in DISC1 C-terminal coiled-coil has GSK3β signaling and sex-dependent behavioral effects in mice.

James Dachtler, Christina Elliott, R John Rodgers, George S Baillie, Steven J Clapcote

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Mutations in DISC1 alter IPNeuronal signaling · 2021
    Review
  6. Review
  7. Frontiers in cellular neuroscience · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The functional variant rs334558 ofPharmacogenomics and personalized medicine · 2018
    Article
  15. Review
  16. Review
  17. Neural Progenitor Cell Polarity and Cortical Development.Frontiers in cellular neuroscience · 2017
    Article
  18. 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

5 authors at 2 institutions in 1 country.

James DachtlerSchool of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, UK.
Christina ElliottInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow G12 8QQ, UK.
R John RodgersInstitute of Psychological Sciences, University of Leeds, Leeds LS2 9JT, UK.
George S BaillieInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow G12 8QQ, UK.
Steven J ClapcoteSchool of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, UK.
University of Leeds · GBUniversity of Glasgow · GB

Funding

Medical Research Council G0900625Medical Research Council MR/J007412/1Wellcome Trust
6 · The paper itself

Abstract

Disrupted-in-Schizophrenia 1 (DISC1) is a risk factor for schizophrenia and affective disorders. The full-length DISC1 protein consists of an N-terminal 'head' domain and a C-terminal tail domain that contains several predicted coiled-coils, structural motifs involved in protein-protein interactions. To probe the in vivo effects of missense mutation of DISC1's C-terminal tail, we tested mice carrying mutation D453G within a predicted α-helical coiled-coil region. We report that, relative to wild-type littermates, female DISC1(D453G) mice exhibited novelty-induced hyperlocomotion, an anxiogenic profile in the elevated plus-maze and open field tests, and reduced social exploration of unfamiliar mice. Male DISC1(D453G) mice displayed a deficit in passive avoidance, while neither males nor females exhibited any impairment in startle reactivity or prepulse inhibition. Whole brain homogenates showed normal levels of DISC1 protein, but decreased binding of DISC1 to GSK3β, decreased phospho-inhibition of GSK3β at serine 9, and decreased levels of β-catenin in DISC1(D453G) mice of either sex. Interrupted GSK3β signaling may thus be part of the mechanism underlying the behavioral phenotype associated with D453G, in common with the previously described N-terminal domain mutations Q31L and L100P in mice, and the schizophrenia risk-conferring variant R264Q in humans.

Indexed as

Behavior, AnimalMutation, MissenseSignal TransductionAmino Acid SequenceAnimalsAnxietyAvoidance LearningDNA Mutational AnalysisFemaleGlycogen Synthase Kinase 3 betaHyperkinesisMaleMiceModels, BiologicalMotor ActivityNerve Tissue ProteinsDisc1 protein, mouseGlycogen Synthase Kinase 3 betaNerve Tissue Proteins

Identifiers

PMID26728762
PMCPMC4700527
OpenAlexW2228305417

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.