ArticlePloS one2014
Whole-genome pathway analysis on 132,497 individuals identifies novel gene-sets associated with body mass index.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Increased adiposity, inflammation, metabolic disruption and dyslipidemia in adult male offspring of DOSS treated C57BL/6 dams.Scientific reports · 2019Article
- A targeted approach to genome-wide studies reveals new genetic associations with central corneal thickness.Molecular vision · 2017Article
- Advancement in genetic variants conferring obesity susceptibility from genome-wide association studies.Frontiers of medicine · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Whole genome pathway analysis is a powerful tool for the exploration of the combined effects of gene-sets within biological pathways. This study applied Interval Based Enrichment Analysis (INRICH) to perform whole-genome pathway analysis of body-mass index (BMI). We used a discovery set composed of summary statistics from a meta-analysis of 123,865 subjects performed by the GIANT Consortium, and an independent sample of 8,632 subjects to assess replication of significant pathways. We examined SNPs within nominally significant pathways using linear mixed models to estimate their contribution to overall BMI heritability. Six pathways replicated as having significant enrichment for association after correcting for multiple testing, including the previously unknown relationships between BMI and the Reactome regulation of ornithine decarboxylase pathway, the KEGG lysosome pathway, and the Reactome stabilization of P53 pathway. Two non-overlapping sets of genes emerged from the six significant pathways. The clustering of shared genes based on previously identified protein-protein interactions listed in PubMed and OMIM supported the relatively independent biological effects of these two gene-sets. We estimate that the SNPs located in examined pathways explain ∼20% of the heritability for BMI that is tagged by common SNPs (3.35% of the 16.93% total).
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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.