Evidence map›Paper›PMID 29667298›Full record

ArticleGenes, brain, and behavior2019

Distinct chromatin structures at the monoamine oxidase-A promoter correlate with allele-specific expression in SH-SY5Y cells.

M Manca, V Pessoa, P Myers, A Pickles, J Hill, H Sharp, C Murgatroyd, V J Bubb, J P Quinn

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes, brain, and behavior, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 27% 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Variable number tandem repeats - Their emerging role in sickness and health.Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  4. 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

9 authors at 4 institutions in 1 country.

M MancaDepartment of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
V PessoaDepartment of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
P MyersDepartment of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
A PicklesKing's College London, MRC Social Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, London, UK.
J HillSchool for Psychology and Clinical Language Sciences, University of Reading, Reading, UK.
H SharpInstitute of Psychology, Health and Society, University of Liverpool, Liverpool, UK.
C MurgatroydSchool of Healthcare Science, Manchester Metropolitan University, Manchester, UK.
V J BubbDepartment of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
J P QuinnDepartment of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.ORCID 0000-0003-3551-7803
University of Liverpool · GBKing's College London · GBManchester Metropolitan University · GBUniversity of Reading · GB

Funding

Medical Research Council G0400577Wellcome Trust
6 · The paper itself

Abstract

Monoamine oxidase-A (MAOA) metabolises monoamines and is implicated in the pathophysiology of psychiatric disorders. A polymorphic repetitive DNA domain, termed the uVNTR (upstream variable number tandem repeat), located at the promoter of the MAOA gene is a risk factor for many of these disorders. MAOA is on the X chromosome suggesting gender could play a role in regulation. We analysed MAOA regulation in the human female cell line, SH-SY5Y, which is polymorphic for the uVNTR. This heterozygosity allowed us to correlate allele-specific gene expression with allele-specific transcription factor binding and epigenetic marks for MAOA. Gene regulation was analysed under basal conditions and in response to the mood stabiliser sodium valproate. Both alleles were transcriptionally active under basal growth conditions; however, the alleles showed distinct transcription factor binding and epigenetic marks at their respective promoters. Exposure of the cells to sodium valproate resulted in differential allelic expression which correlated with allele-specific changes in distinct transcription factor binding and epigenetic marks at the region encompassing the uVNTR. Biochemically our model for MAOA promoter function has implications for gender differences in gene × environment responses in which the uVNTR has been implicated as a genetic risk.

Indexed as

AllelesPromoter Regions, GeneticAntimanic AgentsCell Line, TumorChromatinEpigenesis, GeneticHumansMonoamine OxidaseNeuronsTranscriptional ActivationTranscription FactorsValproic AcidAntimanic AgentsChromatinMonoamine OxidaseTranscription FactorsValproic Acidchromatinepigeneticsgendergene expressionMAOAmental healthtranscriptionVNTRX chromosomeX inactivation

Identifiers

PMID29667298
PMCPMC6617726
OpenAlexW2799463622

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.