Evidence map›Paper›PMID 25549968›Full record

ArticleMolecular systems biology2014

Integrated systems analysis reveals a molecular network underlying autism spectrum disorders.

Jingjing Li, Minyi Shi, Zhihai Ma, Shuchun Zhao, Ghia Euskirchen, Jennifer Ziskin, Alexander Urban, Joachim Hallmayer, Michael Snyder

Open access · goldAbstract read
In one paragraph

Article in Molecular systems biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

82 citing papers in PubMed, 136 citations in OpenAlex.

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  17. The dark side of synaptic proteins in tumours.British journal of cancer · 2022
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22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Jingjing LiDepartment of Genetics, Stanford Center for Genomics and Personalized Medicine Stanford University School of Medicine, Stanford, CA, USA.
Minyi ShiDepartment of Genetics, Stanford Center for Genomics and Personalized Medicine Stanford University School of Medicine, Stanford, CA, USA.
Zhihai MaDepartment of Genetics, Stanford Center for Genomics and Personalized Medicine Stanford University School of Medicine, Stanford, CA, USA.
Shuchun ZhaoDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Ghia EuskirchenDepartment of Genetics, Stanford Center for Genomics and Personalized Medicine Stanford University School of Medicine, Stanford, CA, USA.
Jennifer ZiskinDepartment of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
Alexander UrbanDepartment of Psychiatry & Behavioral Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Joachim HallmayerDepartment of Psychiatry & Behavioral Sciences, Stanford University School of Medicine, Stanford, CA, USA.
Michael SnyderDepartment of Genetics, Stanford Center for Genomics and Personalized Medicine Stanford University School of Medicine, Stanford, CA, USA mpsnyder@stanford.edu.
Stanford University · USStanford Medicine · US

Funding

Special EquipmentP50HG007735 · NHGRI · STANFORD UNIVERSITY · PI CHANG, HOWARD Y · 2014 to 2018
$15.2M
Genomic and epigenomic effects of large CNV in neurons from iPSCDP2MH100010 · NIMH · STANFORD UNIVERSITY · PI URBAN, ALEXANDER ECKEHART · 2012 to 2012
$2.4M
NHGRI NIH HHS P50 HG007735NIMH NIH HHS DP2 MH100010
6 · The paper itself

Abstract

Autism is a complex disease whose etiology remains elusive. We integrated previously and newly generated data and developed a systems framework involving the interactome, gene expression and genome sequencing to identify a protein interaction module with members strongly enriched for autism candidate genes. Sequencing of 25 patients confirmed the involvement of this module in autism, which was subsequently validated using an independent cohort of over 500 patients. Expression of this module was dichotomized with a ubiquitously expressed subcomponent and another subcomponent preferentially expressed in the corpus callosum, which was significantly affected by our identified mutations in the network center. RNA-sequencing of the corpus callosum from patients with autism exhibited extensive gene mis-expression in this module, and our immunochemical analysis showed that the human corpus callosum is predominantly populated by oligodendrocyte cells. Analysis of functional genomic data further revealed a significant involvement of this module in the development of oligodendrocyte cells in mouse brain. Our analysis delineates a natural network involved in autism, helps uncover novel candidate genes for this disease and improves our understanding of its molecular pathology.

Indexed as

Gene Regulatory NetworksGenome, HumanSystems BiologyAnimalsAutism Spectrum DisorderCase-Control StudiesCohort StudiesCorpus CallosumGene ExpressionHumansMaleMiceOligodendrogliaProtein Interaction MapsReproducibility of ResultsSequence Analysis, DNAautism spectrum disorderscorpus callosumfunctional modulesoligodendrocytesprotein interaction network

Identifiers

PMID25549968
PMCPMC4300495
OpenAlexW2098734267

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.