Evidence map›Paper›PMID 23904455›Full record

ArticleHuman molecular genetics2013

Transcriptome study of differential expression in schizophrenia.

Alan R Sanders, Harald H H Göring, Jubao Duan, Eugene I Drigalenko, Winton Moy, Jessica Freda, Deli He, Jianxin Shi, MGS, Pablo V Gejman

Abstract read
In one paragraph

Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 3 pooled it
7.2field-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

52 citing papers in PubMed, 3 syntheses or guidelines pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. A molecular mechanism mediating clozapine-enhanced sensorimotor gating.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
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  11. Review
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  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Double-Edged Sword of Tumour Suppressor Genes in Schizophrenia.Frontiers in molecular neuroscience · 2019
    Review
  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

10 authors at 4 institutions in 1 country.

Alan R SandersDepartment of Psychiatry and Behavioral Sciences, NorthShore University HealthSystem, Evanston, IL 60201, USA.
Harald H H Göring
Jubao Duan
Eugene I Drigalenko
Winton Moy
Jessica Freda
Deli He
Jianxin Shi
MGS
Pablo V Gejman
NorthShore University HealthSystem · USTexas Biomedical Research Institute · USUniversity of Chicago · USNational Cancer Institute · US

Funding

AN NCRR CENTER FOR HIGH THROUGHPUT SNP GENOTYPING AND ANALYSIS: GAIN NETWORKU54RR020278 · NCRR · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GABRIEL, STACEY · 2004 to 2008
$14.4M
MOLECULAR GENETICS OF SCHIZOPHRENIAR01MH059571 · NIMH · UNIVERSITY OF CHICAGO · PI GEJMAN, PABLO V. · 1999 to 2007
$8.0M
A Genome-Wide Association Study of SchizophreniaU01MH079469 · NIMH · NORTHSHORE UNIVERSITY HEALTHSYSTEM · PI GEJMAN, PABLO V. · 2007 to 2009
$4.4M
EXTRAMULAR RESEARCH FACILITIES CONSTRUCTIONC06RR017515 · NCRR · SOUTHWEST FOUNDATION FOR BIOMEDICAL RES · PI SHADE, ROBERT E · 2003 to 2003
$3.1M
MOLECULAR GENETICS OF SCHIZOPHRENIAR01MH060879 · NIMH · WASHINGTON UNIVERSITY · PI CLONINGER, C. ROBERT · 1999 to 2006
$2.7M
Joint Mapping of Genome-Wide Gene Expression and Association in a Schizophrenia DRC2MH090030 · NIMH · ENDEAVOR HEALTH CLINICAL OPERATIONS · PI SANDERS, ALAN R · 2009 to 2010
$2.0M
MOLECULAR GENETICS OF SCHIZOPHRENIAR01MH059586 · NIMH · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI SILVERMAN, JEREMY M. · 1999 to 2006
$1.9M
MOLECULAR GENETICS OF SCHIZOPHRENIAR01MH061675 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI LEVINSON, DOUGLAS FREDERICK · 1999 to 2007
$1.8M
MOLECULAR GENETICS OF SCHIZOPHRENIAR01MH059587 · NIMH · EMORY UNIVERSITY · PI AMIN, FAROOQ · 1999 to 2006
$1.8M
MOLECULAR GENETICS OF SCHIZOPHRENIAR01MH059565 · NIMH · UNIVERSITY OF COLORADO DENVER · PI FREEDMAN, ROBERT · 1999 to 2006
$1.7M
MOLECULAR GENETICS OF SCHIZOPHRENIAR01MH059588 · NIMH · UNIVERSITY OF QUEENSLAND · PI MOWRY, BRYAN JOHN · 1999 to 2006
$1.4M
MOLECULAR GENETICS OF SCHIZOPHRENIAR01MH060870 · NIMH · UNIVERSITY OF CALIFORNIA IRVINE · PI BYERLEY, WILLIAM · 1999 to 2006
$1.3M
NCRR NIH HHS C06 RR017515NCRR NIH HHS RR017515NCRR NIH HHS U54 RR020278NCRR NIH HHS U54RR020278NIMH NIH HHS R01MH059565NIMH NIH HHS R01MH059566NIMH NIH HHS R01MH059571NIMH NIH HHS R01MH059586NIMH NIH HHS R01MH059587NIMH NIH HHS R01MH059588NIMH NIH HHS R01MH060870NIMH NIH HHS R01MH060879NIMH NIH HHS R01MH061675NIMH NIH HHS R01MH067257NIMH NIH HHS R01MH081800NIMH NIH HHS RC2 MH090030NIMH NIH HHS RC2MH090030NIMH NIH HHS U01MH046276NIMH NIH HHS U01MH046289NIMH NIH HHS U01MH046318NIMH NIH HHS U01MH079469NIMH NIH HHS U01MH079470
6 · The paper itself

Abstract

Schizophrenia genome-wide association studies (GWAS) have identified common SNPs, rare copy number variants (CNVs) and a large polygenic contribution to illness risk, but biological mechanisms remain unclear. Bioinformatic analyses of significantly associated genetic variants point to a large role for regulatory variants. To identify gene expression abnormalities in schizophrenia, we generated whole-genome gene expression profiles using microarrays on lymphoblastoid cell lines (LCLs) from 413 cases and 446 controls. Regression analysis identified 95 transcripts differentially expressed by affection status at a genome-wide false discovery rate (FDR) of 0.05, while simultaneously controlling for confounding effects. These transcripts represented 89 genes with functions such as neurotransmission, gene regulation, cell cycle progression, differentiation, apoptosis, microRNA (miRNA) processing and immunity. This functional diversity is consistent with schizophrenia's likely significant pathophysiological heterogeneity. The overall enrichment of immune-related genes among those differentially expressed by affection status is consistent with hypothesized immune contributions to schizophrenia risk. The observed differential expression of extended major histocompatibility complex (xMHC) region histones (HIST1H2BD, HIST1H2BC, HIST1H2BH, HIST1H2BG and HIST1H4K) converges with the genetic evidence from GWAS, which find the xMHC to be the most significant susceptibility locus. Among the differentially expressed immune-related genes, B3GNT2 is implicated in autoimmune disorders previously tied to schizophrenia risk (rheumatoid arthritis and Graves' disease), and DICER1 is pivotal in miRNA processing potentially linking to miRNA alterations in schizophrenia (e.g. MIR137, the second strongest GWAS finding). Our analysis provides novel candidate genes for further study to assess their potential contribution to schizophrenia.

Indexed as

Gene Expression RegulationTranscriptomeAdultCase-Control StudiesCell LineFemaleGene Regulatory NetworksGenome-Wide Association StudyHumansMaleMiddle AgedMolecular Sequence AnnotationPolymorphism, Single NucleotideQuantitative Trait LociSchizophreniaSignal Transduction

Identifiers

PMID23904455
PMCPMC3836479
OpenAlexW2132123917

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.