Evidence map›Paper›PMID 24135908›Full record

ReviewHuman genetics2014

Genomics meets proteomics: identifying the culprits in disease.

Hendrik G Stunnenberg, Nina C Hubner

Abstract readReview
In one paragraph

Review in Human genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Pediatric asthma and autism-genomic perspectives.Clinical and translational medicine · 2015
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
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

2 authors.

Hendrik G StunnenbergDepartment of Molecular Biology, Faculty of Science, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen, 6525 GA, Nijmegen, The Netherlands.
Nina C Hubner

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome-wide association studies (GWAS) revealed genomic risk loci that potentially have an impact on disease and phenotypic traits. This extensive resource holds great promise in providing novel directions for personalized medicine, including disease risk prediction, prevention and targeted medication. One of the major challenges that researchers face on the path between the initial identification of an association and precision treatment of patients is the comprehension of the biological mechanisms that underlie these associations. Currently, the focus to solve these questions lies on the integrative analysis of system-wide data on global genome variation, gene expression, transcription factor binding, epigenetic profiles and chromatin conformation. The generation of this data mainly relies on next-generation sequencing. However, due to multiple recent developments, mass spectrometry-based proteomics now offers additional, by the GWAS field so far hardly recognized possibilities for the identification of functional genome variants and, in particular, for the identification and characterization of (differentially) bound protein complexes as well as physiological target genes. In this review, we introduce these proteomics advances and suggest how they might be integrated in post-GWAS workflows. We argue that the combination of highly complementary techniques is powerful and can provide an unbiased, detailed picture of GWAS loci and their mechanistic involvement in disease.

Indexed as

Genome, HumanChromatinEpigenesis, GeneticGenetic LociGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyGenomicsHigh-Throughput Nucleotide SequencingHumansPrecision MedicineProteomeTandem Mass SpectrometryChromatinProteome

Identifiers

PMID24135908
PMCPMC4021166

What OpenQuestion holds

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LicenceCC BY
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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.