Evidence map›Paper›PMID 26440730›Full record

ArticleThe pharmacogenomics journal2016

Analysis of the effects of depression associated polymorphisms on the activity of the BICC1 promoter in amygdala neurones.

S Davidson, L Shanley, P Cowie, M Lear, P McGuffin, J P Quinn, P Barrett, A MacKenzie

Open access · hybridAbstract read
In one paragraph

Article in The pharmacogenomics journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 15% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Non-coding genetic variation shaping mental health.Current opinion in psychology · 2019
    Review
  8. Review
  9. 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 3 institutions in 1 country.

S DavidsonSchool of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, UK.
L ShanleySchool of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, UK.
P CowieSchool of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, UK.
M LearSchool of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, UK.
P McGuffinSocial, Genetic and Developmental Psychiatry Centre (MRC), Institute of Psychiatry, Psychology and Neuroscience, Denmark Hill, London, UK.
J P QuinnDepartment of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
P BarrettThe Rowett Institute of Nutrition and Health, Bucksburn, Aberdeen, UK.
A MacKenzieSchool of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, UK.
University of Aberdeen · GBPsychiatry Research Trust · GBUniversity of Liverpool · GB

Funding

Biotechnology and Biological Sciences Research Council BB/D004659/1Medical Research Council G0701003Wellcome TrustWellcome Trust 080980
6 · The paper itself

Abstract

The Bicaudal C Homolog 1 (BICC1) gene, which encodes an RNA binding protein, has been identified by genome wide association studies (GWAS) as a candidate gene associated with major depressive disorder (MDD). We explored the hypothesis that MDD associated single-nucleotide polymorphisms (SNPs) affected the ability of cis-regulatory elements within intron 3 of the BICC1 gene to modulate the activity of the BICC1 promoter region. We initially established that the BICC1 promoter drove BICC1 mRNA expression in amygdala, hippocampus and hypothalamus. Intriguingly, we provide evidence that MDD associated polymorphisms alter the ability of the BICC1 promoter to respond to PKA signalling within amygdala neurones. Considering the known role of amygdala PKA pathways in fear learning and mood these observations suggest a possible mechanism through which allelic changes in the regulation of the BICC1 gene in amygdala neurones may contribute to mood disorders. Our findings also suggest a novel direction for the identification of novel drug targets and the design of future personalised therapeutics.The Pharmacogenomics Journal advance online publication, 6 October 2015; doi:10.1038/tpj.2015.62.

Indexed as

Polymorphism, Single NucleotidePromoter Regions, GeneticAffectAmygdalaAnimalsBinding SitesCells, CulturedComputational BiologyCyclic AMP-Dependent Protein KinasesEnzyme ActivationHumansIntronsLinkage DisequilibriumMajor Depressive DisorderMice, Inbred C57BLMice, Inbred CBABicc1 protein, humanCyclic AMP-Dependent Protein KinasesRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID26440730
PMCPMC4973013
OpenAlexW2208207554

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.