Evidence map›Paper›PMID 20480378›Full record

ArticleJournal of neural transmission (Vienna, Austria : 1996)2010

The expression of the transcription factor FEV in adult human brain and its association with affective disorders.

Claudia B Kriegebaum, Lise Gutknecht, Lena Bartke, Andreas Reif, Henriette N Buttenschon, Ole Mors, Klaus-Peter Lesch, Angelika G Schmitt

Abstract read
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In one paragraph

Article in Journal of neural transmission (Vienna, Austria : 1996), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Comparative structure analysis of the ETSi domain of ERG3 and its complex with the E74 promoter DNA sequence.Acta crystallographica. Section F, Structural biology communications · 2018
    Article
  6. Review
  7. Review
  8. Brain serotonergic circuitries.Dialogues in clinical neuroscience · 2010
    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

8 authors at 2 institutions in 2 countries.

Claudia B KriegebaumMolecular and Clinical Psychobiology, Department of Psychiatry, Psychosomatics and Psychotherapy, University of Würzburg, Füchsleinstr. 15, 97080, Würzburg, Germany. claudia.kriegebaum@web.de
Lise Gutknecht
Lena Bartke
Andreas Reif
Henriette N Buttenschon
Ole Mors
Klaus-Peter Lesch
Angelika G Schmitt
University of Würzburg · DEAarhus University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A wide range of physiological processes and neuronal functioning is modulated by the serotonergic system. Serotonin (5-HT) plays an important role during early brain development. Moreover, dysfunction of the 5-HT system is implicated in psychiatric disorders, especially in affective disorders. Little is known, however, about the transcriptional mechanisms leading to a functional 5-HT system in humans. The Fifth Ewing Variant (FEV), an E-twenty-six (ETS) transcription factor, is assumed to be involved in the transcription of gene(s) in the serotonergic pathway and to play a role in early brain development. To investigate its specificity, we performed an expression analysis of FEV in different human brain regions utilizing quantitative real-time polymerase chain reaction. Our results demonstrate that FEV is not exclusively expressed in serotonergic neurons, but, on the contrary, also in several non-serotonergic brain regions such as locus coeruleus, caudate nucleus and putamen. In the latter two regions, FEV expression levels actually were higher when compared with the pons and the medulla oblongata, which contain the raphe nuclei. Additionally, we examined whether genetic variance in the FEV gene contributes to the susceptibility towards affective disorders. Direct re-sequencing, however, did not provide evidence for FEV mutations in patients, and neither were non-coding single nucleotide polymorphisms associated with disease. FEV therefore might not account for the genetic risk towards depression or bipolar disorder. Furthermore, the specificity of FEV for the serotonergic system should be reconsidered.

Indexed as

AdolescentAdultAgedBipolar DisorderBrainCase-Control StudiesDepressive DisorderDNA-Binding ProteinsFemaleGene FrequencyGenetic Predisposition to DiseaseHumansLinkage DisequilibriumMaleMiddle AgedMood DisordersDNA-Binding ProteinsFEV protein, humanNuclear ProteinsRNA, MessengerTranscription Factors

Identifiers

PMID20480378
OpenAlexW2000827148

What OpenQuestion holds

Textmetadata
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.