ArticleCell2019
Trans Effects on Gene Expression Can Drive Omnigenic Inheritance.
Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 340 papers, 3 of them syntheses that pooled 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.
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.
Who cites it
340 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Trans-eQTL mapping prioritises USP18 as a negative regulator of interferon response at a lupus risk locus.Nature communications · 2025Pooled it
- Pooled it
- FHL5 Controls Vascular Disease-Associated Gene Programs in Smooth Muscle Cells.Circulation research · 2023Pooled it
- The role ofEpigenetics · 2026Review
- CRISPR decodes the RNA regulatory network in prostate cancer: A review from mechanisms to precision therapeutics.Non-coding RNA research · 2026Review
- Translating functional molecular knowledge into crop-breeding success.Nature reviews. Genetics · 2026Review
- Genetic landscape of an in vivo protein interactome.Nature genetics · 2026Article
- Polygenic risk scores and plasma proteomics identify cancer-related proteins and trans-regulated protein networks.Cell genomics · 2026Article
- Genetic architectures of brain-related traits are shaped by strong selective constraints.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cell-type specific analyses in blood and gut identify cis-eQTL matching 140 IBD risk loci and entrectinib as repurposing candidate.Nature communications · 2026Article
- Article
- Partitioned blood pressure polygenic risk reveals differential genetic effects of tissue-specific enhancers and their interactions on cardiovascular disease.Research square · 2026Article
- Article
- Article
- Network Properties Influence Covariance Between Gene Expression and Fecundity Fitness of Caenorhabditis elegans in a Novel Laboratory Environment.Genome biology and evolution · 2026Article
- Evolutionary adaptation proceeds through a small number of phenotypic modules.Molecular biology and evolution · 2026Article
- Robustly enhancing crop genomic prediction accuracy through ensemble learning and iterative optimization.Nature communications · 2026Article
- From GWAS Signals to Molecular Mechanisms: Explainable AI for Causal Gene Prioritization and Biomolecular Target Interpretation.Biomolecules · 2026Review
- Co-expression-based models improve eQTL predictions for transcriptome-wide association studies and highlight new schizophrenia-associated genes.Nature genetics · 2026Article
- Optimized phenotype definitions boost GWAS power.PLoS computational biology · 2026Article
280 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Early genome-wide association studies (GWASs) led to the surprising discovery that, for typical complex traits, most of the heritability is due to huge numbers of common variants with tiny effect sizes. Previously, we argued that new models are needed to understand these patterns. Here, we provide a formal model in which genetic contributions to complex traits are partitioned into direct effects from core genes and indirect effects from peripheral genes acting in trans. We propose that most heritability is driven by weak trans-eQTL SNPs, whose effects are mediated through peripheral genes to impact the expression of core genes. In particular, if the core genes for a trait tend to be co-regulated, then the effects of peripheral variation can be amplified such that nearly all of the genetic variance is driven by weak trans effects. Thus, our model proposes a framework for understanding key features of the architecture of complex traits.
Indexed as
Identifiers
What OpenQuestion holds
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.