Evidence map›Paper›PMID 20433909›Full record

ReviewBrain research bulletin2010

Neuregulin 1-erbB4 pathway in schizophrenia: From genes to an interactome.

Anamika Banerjee, Mathew L Macdonald, Karin E Borgmann-Winter, Chang-Gyu Hahn

Open access · greenAbstract readReview
In one paragraph

Review in Brain research bulletin, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Review
  3. Cortical myelin mapping in antipsychotic medication-naïve, first-episode psychosis patients.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Laser capture microdissection-targeted mass spectrometry: a method for multiplexed protein quantification within individual layers of the cerebral cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  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

4 authors at 1 institution in 1 country.

Anamika BanerjeeDepartment of Psychiatry, University of Pennsylvania, Philadelphia, PA 19104-3403, United States.
Mathew L Macdonald
Karin E Borgmann-Winter
Chang-Gyu Hahn
University of Pennsylvania · US

Funding

Src mediates molecular alterations leading to NMDAR hypofunction in schizophreniaR01MH075916 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI BORGMANN-WINTER, KARIN, HAHN, CHANG-GYU · 2006 to 2019
$3.3M
NIMH NIH HHS R01 MH075916
6 · The paper itself

Abstract

Recently identified candidate susceptibility genes for schizophrenia are likely to play, important roles in the pathophysiology of the illness. It is also clear, however, that the etiologic, contribution of these genes is not only via their own functions but also through interactions with other, genes and environmental factors. Genetic, transgenic and postmortem brain studies support a, potential role for NRG1-erbB4 signaling in schizophrenia. Embedded in the results of these studies, however, are clues to the notion that NRG1-erbB4 signaling does not act alone but in conjunction with, other pathways. This article aims to re-evaluate the evidence for the role of neuregulin 1 (NRG1)-erbB4 signaling in schizophrenia by focusing on its interactions with other candidate susceptibility, pathways. In addition, we consider molecular substrates upon which the NRG1-erbB4 and other, candidate pathways converge contributing to susceptibility for the illness (schizophrenia interactome). Glutamatergic signaling can be an interesting candidate for schizophrenia interactome. Schizophrenia is associated with NMDA receptor hypofunction and moreover, several susceptibility genes for, schizophrenia converge on NMDA receptor signaling. These candidate genes influence NMDA receptor, signaling via diverse mechanisms, yet all eventually impact on protein composition of NMDA receptor, complexes. Likewise, the protein associations in the receptor complexes can themselves modulate, signaling molecules of candidate genes and their pathways. Therefore, protein-protein interactions in the NMDA receptor complexes can mediate reciprocal interactions between NMDA receptor function, and susceptibility candidate pathways including NRG1-erbB4 signaling and thus can be a, schizophrenia interactome.

Indexed as

AnimalsErbB ReceptorsHumansNeuregulin-1Receptor, ErbB-4Receptors, N-Methyl-D-AspartateSchizophreniaSignal TransductionERBB4 protein, humanErbB ReceptorsNeuregulin-1Receptor, ErbB-4Receptors, N-Methyl-D-Aspartate

Identifiers

PMID20433909
PMCPMC5050041
OpenAlexW2083669410

What OpenQuestion holds

Textmetadata
LicenceTDM
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.