Evidence map›Paper›PMID 29196732›Full record

ArticleScientific reports2017

Human CRMP4 mutation and disrupted Crmp4 expression in mice are associated with ASD characteristics and sexual dimorphism.

Atsuhiro Tsutiya, Yui Nakano, Emily Hansen-Kiss, Benjamin Kelly, Masugi Nishihara, Yoshio Goshima, Don Corsmeier, Peter White, Gail E Herman, Ritsuko Ohtani-Kaneko

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  4. Review
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  13. International journal of molecular sciences · 2019
    Review
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

10 authors at 4 institutions in 2 countries.

Atsuhiro TsutiyaInstitute of Life Innovation Studies, Toyo University, 1-1-1 Itakura, Oura, Gunma, 374-0193, Japan.
Yui NakanoGraduate School of Life Sciences, Toyo University, 1-1-1 Itakura, Oura, Gunma, 374-0193, Japan.
Emily Hansen-KissThe Institute for Genomic Medicine, Nationwide Children's Hospital and Department of Pediatrics, The Ohio State University, Columbus, OH, 43205, USA.
Benjamin KellyThe Institute for Genomic Medicine, Nationwide Children's Hospital and Department of Pediatrics, The Ohio State University, Columbus, OH, 43205, USA.
Masugi NishiharaDepartment of Veterinary Physiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, 113-8657, Japan.
Yoshio GoshimaDepartment of Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine, 3-9 Fuku-ura, Kanazawa Ward, Yokohama, 236-0004, Japan.
Don CorsmeierThe Institute for Genomic Medicine, Nationwide Children's Hospital and Department of Pediatrics, The Ohio State University, Columbus, OH, 43205, USA.
Peter WhiteThe Institute for Genomic Medicine, Nationwide Children's Hospital and Department of Pediatrics, The Ohio State University, Columbus, OH, 43205, USA.ORCID 0000-0002-5218-5903
Gail E HermanThe Institute for Genomic Medicine, Nationwide Children's Hospital and Department of Pediatrics, The Ohio State University, Columbus, OH, 43205, USA.
Ritsuko Ohtani-KanekoInstitute of Life Innovation Studies, Toyo University, 1-1-1 Itakura, Oura, Gunma, 374-0193, Japan. r-kaneko@toyo.jp.
Nationwide Children's Hospital · USToyo University · JPThe University of Tokyo · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorders (ASD) are more common among boys than girls. The mechanisms responsible for ASD symptoms and their sex differences remain mostly unclear. We previously identified collapsin response mediator protein 4 (CRMP4) as a protein exhibiting sex-different expression during sexual differentiation of the hypothalamic sexually dimorphic nucleus. This study investigated the relationship between the sex-different development of autistic features and CRMP4 deficiency. Whole-exome sequencing detected a de novo variant (S541Y) of CRMP4 in a male ASD patient. The expression of mutated mouse CRMP4

Indexed as

Mutation, MissenseAnimalsAutism Spectrum DisorderCells, CulturedDisease Models, AnimalFemaleGene Expression RegulationGene Knockout TechniquesGenetic Association StudiesHippocampusHumansMaleMiceMuscle ProteinsNerve Tissue ProteinsNeuronsDPYSL3 protein, humanDpysl3 protein, mouseMuscle ProteinsNerve Tissue Proteins

Identifiers

PMID29196732
PMCPMC5711804
OpenAlexW2770300534

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.