Evidence map›Paper›PMID 28240269›Full record

ArticleNature communications2017

Connecting genetic risk to disease end points through the human blood plasma proteome.

Karsten Suhre, Matthias Arnold, Aditya Mukund Bhagwat, Richard J Cotton, Rudolf Engelke, Johannes Raffler, Hina Sarwath, Gaurav Thareja, Annika Wahl, Robert Kirk DeLisle and 14 more

Erratum issued Registry-linked trialAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT06652867 (Hypoglycemia Biomarkers to Predict Timing of a Hypoglycemic Event), which is not on this map. Cited by 528 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
528citing papers in PubMed, 7 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.

NCT06652867 completednot on this mapstarted 2024, after this paper: background citation

Hypoglycemia Biomarkers to Predict Timing of a Hypoglycemic Event

TypeobservationalSponsorRoyal College of Surgeons in Ireland - Medical University of BahrainRan2024 to 2024Enrolled150ConditionsHypoglycemia
3 · Its place in the literature

Who cites it

528 citing papers in PubMed, 7 syntheses or guidelines pooled it.

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  15. Proteogenomics in human populations.Nature reviews. Genetics · 2026
    Review
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468 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors.

Karsten SuhreDepartment of Physiology and Biophysics, Weill Cornell Medicine-Qatar, Education City, PO 24144 Doha, Qatar.ORCID 0000-0001-9638-3912
Matthias ArnoldInstitute of Bioinformatics and Systems Biology, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstraße 1, 85764 Neuherberg, Germany.ORCID 0000-0002-4666-0923
Aditya Mukund BhagwatProteomics Core, Weill Cornell Medicine-Qatar, Education City, PO 24144 Doha, Qatar.
Richard J CottonProteomics Core, Weill Cornell Medicine-Qatar, Education City, PO 24144 Doha, Qatar.
Rudolf EngelkeProteomics Core, Weill Cornell Medicine-Qatar, Education City, PO 24144 Doha, Qatar.
Johannes RafflerInstitute of Bioinformatics and Systems Biology, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstraße 1, 85764 Neuherberg, Germany.
Hina SarwathProteomics Core, Weill Cornell Medicine-Qatar, Education City, PO 24144 Doha, Qatar.
Gaurav TharejaDepartment of Physiology and Biophysics, Weill Cornell Medicine-Qatar, Education City, PO 24144 Doha, Qatar.
Annika WahlResearch Unit of Molecular Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstraße 1, 85764 Neuherberg, Germany.
Robert Kirk DeLisleSomaLogic, 2945 Wilderness Pl, Boulder, Colorado 80301, USA.
Larry GoldSomaLogic, 2945 Wilderness Pl, Boulder, Colorado 80301, USA.
Marija PezerGenos Ltd, Glycoscience Research Laboratory, Hondlova 2/11, 10000 Zagreb, Croatia.ORCID 0000-0002-6480-1427
Gordan LaucGenos Ltd, Glycoscience Research Laboratory, Hondlova 2/11, 10000 Zagreb, Croatia.
Mohammed A El-Din SelimDepartment of Dermatology, Hamad Medical Corporation, PO Box 3050 Doha, Qatar.
Dennis O Mook-KanamoriLeiden University Medical Centre, PO Box 9600, 2300 RC Leiden, The Netherlands.
Eman K Al-DousGenomics Core, Weill Cornell Medicine-Qatar, Education City, PO 24144, Doha, Qatar.
Yasmin A MohamoudGenomics Core, Weill Cornell Medicine-Qatar, Education City, PO 24144, Doha, Qatar.
Joel MalekGenomics Core, Weill Cornell Medicine-Qatar, Education City, PO 24144, Doha, Qatar.
Konstantin StrauchInstitute of Genetic Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstraße 1, 85764 Neuherberg, Germany.
Harald GrallertResearch Unit of Molecular Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstraße 1, 85764 Neuherberg, Germany.
Annette PetersInstitute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstraße 1, 85764 Neuherberg, Germany.
Gabi KastenmüllerInstitute of Bioinformatics and Systems Biology, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstraße 1, 85764 Neuherberg, Germany.
Christian GiegerResearch Unit of Molecular Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstraße 1, 85764 Neuherberg, Germany.
Johannes GraumannProteomics Core, Weill Cornell Medicine-Qatar, Education City, PO 24144 Doha, Qatar.ORCID 0000-0002-3015-5850

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome-wide association studies (GWAS) with intermediate phenotypes, like changes in metabolite and protein levels, provide functional evidence to map disease associations and translate them into clinical applications. However, although hundreds of genetic variants have been associated with complex disorders, the underlying molecular pathways often remain elusive. Associations with intermediate traits are key in establishing functional links between GWAS-identified risk-variants and disease end points. Here we describe a GWAS using a highly multiplexed aptamer-based affinity proteomics platform. We quantify 539 associations between protein levels and gene variants (pQTLs) in a German cohort and replicate over half of them in an Arab and Asian cohort. Fifty-five of the replicated pQTLs are located in trans. Our associations overlap with 57 genetic risk loci for 42 unique disease end points. We integrate this information into a genome-proteome network and provide an interactive web-tool for interrogations. Our results provide a basis for novel approaches to pharmaceutical and diagnostic applications.

Indexed as

Endpoint DeterminationGenetic Predisposition to DiseaseAllelesBlood ProteinsComplement System ProteinsDrug Delivery SystemsGene Regulatory NetworksGenetic VariationGenome, HumanGenome-Wide Association StudyGlycoproteinsHemeHumansMolecular Sequence AnnotationPharmacogeneticsProtein Processing, Post-TranslationalBlood ProteinsComplement System ProteinsGlycoproteinsHemeProteomeRNA, Messenger

Identifiers

PMID28240269
PMCPMC5333359

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.