Evidence map›Paper›PMID 33901562›Full record

ArticleThe Journal of investigative dermatology2021

Triangulating Molecular Evidence to Prioritize Candidate Causal Genes at Established Atopic Dermatitis Loci.

Maria K Sobczyk, Tom G Richardson, Verena Zuber, Josine L Min, Tom R Gaunt, Lavinia Paternoster, eQTLGen Consortium, BIOS Consortium, GoDMC

Abstract read
In one paragraph

Article in The Journal of investigative dermatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

17 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
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  5. Atopic Dermatitis: New Targets and Emerging Systemic Therapies.American journal of clinical dermatology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Maria K SobczykMRC Integrative Epidemiology Unit, Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Tom G RichardsonMRC Integrative Epidemiology Unit, Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Verena ZuberDepartment of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom; MRC Biostatistics Unit, School of Clinical Medicine, University of Cambridge, Cambridge, United Kingdom.
Josine L MinMRC Integrative Epidemiology Unit, Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Tom R GauntMRC Integrative Epidemiology Unit, Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Lavinia PaternosterMRC Integrative Epidemiology Unit, Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom. Electronic address: l.paternoster@bristol.ac.uk.
eQTLGen Consortium, BIOS Consortium, GoDMC

Funding

Medical Research Council MC_UU_00011/4Medical Research Council MC_UU_00011/5Medical Research Council MR/S003886/1Wellcome Trust
6 · The paper itself

Abstract

GWASs for atopic dermatitis have identified 25 reproducible loci. We attempt to prioritize the candidate causal genes at these loci using extensive molecular resources compiled into a bioinformatics pipeline. We identified a list of 103 molecular resources for atopic dermatitis etiology, including expression, protein, and DNA methylation quantitative trait loci datasets in the skin or immune-relevant tissues, which were tested for overlap with GWAS signals. This was combined with functional annotation using regulatory variant prediction and features such as promoter‒enhancer interactions, expression studies, and variant fine mapping. For each gene at each locus, we condensed the evidence into a prioritization score. Across the investigated loci, we detected significant enrichment of genes with adaptive immune regulatory function and epidermal barrier formation among the top-prioritized genes. At eight loci, we were able to prioritize a single candidate gene (IL6R, ADO, PRR5L, IL7R, ETS1, INPP5D, MDM1, TRAF3). In addition, at 6 of the 25 loci, our analysis prioritizes less familiar candidates (SLC22A5, IL2RA, MDM1, DEXI, ADO, STMN3). Our analysis provides support for previously implicated genes at several atopic dermatitis GWAS loci as well as evidence for plausible additional candidates at others, which may represent potential targets for drug discovery.

Indexed as

Genetic LociGenome-Wide Association StudyDermatitis, AtopicHumansQuantitative Trait Loci

Identifiers

PMID33901562
PMCPMC8592116

What OpenQuestion holds

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Registered trials

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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.