ArticleBiology letters2022
Modelling the genetic aetiology of complex disease: human-mouse conservation of noncoding features and disease-associated loci.
Article in Biology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- Functional genomics in age-related macular degeneration: From genetic associations to understanding disease mechanisms.Experimental eye research · 2025Review
- Antibody-based alternatives to animal testing for toxin detection and antitoxin evaluation.Frontiers in toxicology · 2025Review
- The genetics of adipose tissue metabolism.Royal Society open science · 2024Article
- Learning functional conservation between human and pig to decipher evolutionary mechanisms underlying gene expression and complex traits.Cell genomics · 2023Article
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Authors and funding
7 authors.
Funding
Abstract
Understanding the genetic aetiology of loci associated with a disease is crucial for developing preventative measures and effective treatments. Mouse models are used extensively to understand human pathobiology and mechanistic functions of disease-associated loci. However, the utility of mouse models is limited in part by evolutionary divergence in transcription regulation for pathways of interest. Here, we summarize the alignment of genomic (exonic and multi-cell regulatory) annotations alongside Mendelian and complex disease-associated variant sites between humans and mice. Our results highlight the importance of understanding evolutionary divergence in transcription regulation when interpreting functional studies using mice as models for human disease variants.
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