Evidence map›Paper›PMID 22832403›Full record

ArticleTranslational psychiatry2011

Increased expression of receptor phosphotyrosine phosphatase-β/ζ is associated with molecular, cellular, behavioral and cognitive schizophrenia phenotypes.

N Takahashi, T Sakurai, O Bozdagi-Gunal, N P Dorr, J Moy, L Krug, M Gama-Sosa, G A Elder, R J Koch, R H Walker and 3 more

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

33 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Phosphatase Signaling as a Therapeutic Strategy in Schizophrenia.International journal of molecular sciences · 2026
    Review
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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

13 authors at 3 institutions in 2 countries.

N TakahashiDepartment of Psychiatry, Mount Sinai School of Medicine, New York, NY 10029, USA.
T Sakurai
O Bozdagi-Gunal
N P Dorr
J Moy
L Krug
M Gama-Sosa
G A Elder
R J Koch
R H Walker
P R Hof
K L Davis
J D Buxbaum
Icahn School of Medicine at Mount Sinai · USAllen Institute for Brain Science · USJames J. Peters VA Medical Center · US

Funding

White Matter Abnormalities in SchizophreniaP50MH066392 · NIMH · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI O'DONOVAN, MICHAEL J · 2002 to 2012
$18.6M
NIMH NIH HHS P50 MH066392
6 · The paper itself

Abstract

Schizophrenia is a serious and chronic mental disorder, in which both genetic and environmental factors have a role in the development of the disease. Neuregulin-1 (NRG1) is one of the most established genetic risk factors for schizophrenia, and disruption of NRG1 signaling has been reported in this disorder. We reported previously that NRG1/ErbB4 signaling is inhibited by receptor phosphotyrosine phosphatase-β/ζ (RPTP β/ζ) and that the gene encoding RPTPβ/ζ (PTPRZ1) is genetically associated with schizophrenia. In this study, we examined the expression of RPTPβ/ζ in the brains of patients with schizophrenia and observed increased expression of this gene. We developed mice overexpressing RPTPβ/ζ (PTPRZ1-transgenic mice), which showed reduced NRG1 signaling, and molecular and cellular changes implicated in the pathogenesis of schizophrenia, including altered glutamatergic, GABAergic and dopaminergic activity, as well as delayed oligodendrocyte development. Behavioral analyses also demonstrated schizophrenia-like changes in the PTPRZ1-transgenic mice, including reduced sensory motor gating, hyperactivity and working memory deficits. Our results indicate that enhanced RPTPβ/ζ signaling can contribute to schizophrenia phenotypes, and support both construct and face validity for PTPRZ1-transgenic mice as a model for multiple schizophrenia phenotypes. Furthermore, our results implicate RPTPβ/ζ as a therapeutic target in schizophrenia.

Indexed as

Gene Expression Regulation, EnzymologicPhenotypeAdultAnimalsCognition DisordersDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLMice, TransgenicMiddle AgedReceptor-Like Protein Tyrosine Phosphatases, Class 5SchizophreniaSignal TransductionReceptor-Like Protein Tyrosine Phosphatases, Class 5

Identifiers

PMID22832403
PMCPMC3309478
OpenAlexW2082702433

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.