ReviewCurrent opinion in genetics & development2013
Edgotype: a fundamental link between genotype and phenotype.
Review in Current opinion in genetics & development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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
90 citing papers in PubMed, 158 citations in OpenAlex.
- Peroxisomal interactome mapping enables network-based modelling of function and disease.Life science alliance · 2026Article
- Human genetics across levels of biological organization.Nature reviews. Genetics · 2026Review
- Predicting interaction-specific protein-protein interaction perturbations by missense variants with MutPred-PPI.bioRxiv : the preprint server for biology · 2026Article
- Vertebral morphological changes driven byZoological research · 2026Article
- Molecular interplay between glycogen synthase kinase 3 beta and A-kinase anchoring protein 11 in bipolar disorder: a narrative review.Frontiers in molecular neuroscience · 2026Review
- Sliding Window Interaction Grammar (SWING): a generalized interaction language model for peptide and protein interactions.Nature methods · 2025Article
- A quantitative comparison of the deleteriousness of missense and nonsense mutations using the structurally resolved human protein interactome.Protein science : a publication of the Protein Society · 2025Article
- Disentangling the mutational effects on protein stability and interaction of human MLH1.PLoS genetics · 2025Article
- Single-cell network biology enabling cell-type-resolved disease genetics.Genomics & informatics · 2025Review
- Article
- Article
- Uncovering cell-type-specific immunomodulatory variants and molecular phenotypes in COVID-19 using structurally resolved protein networks.Cell reports · 2024Article
- Article
- Ubiquitin: Not just a one-way ticket to the proteasome, but a therapeutic dial to fine-tune the molecular landscape of disease.Clinical and translational medicine · 2024Review
- The Extent of Edgetic Perturbations in the Human Interactome Caused by Population-Specific Mutations.Biomolecules · 2023Article
- Neurolysin Knockout Mice in a Diet-Induced Obesity Model.International journal of molecular sciences · 2023Article
- Pervasive mislocalization of pathogenic coding variants underlying human disorders.bioRxiv : the preprint server for biology · 2023Article
- Phenotypic heterogeneity in human genetic diseases: ultrasensitivity-mediated threshold effects as a unifying molecular mechanism.Journal of biomedical science · 2023Review
- Review
- AD-Syn-Net: systematic identification of Alzheimer's disease-associated mutation and co-mutation vulnerabilities via deep learning.Briefings in bioinformatics · 2023Article
30 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
7 authors at 2 institutions in 1 country.
Funding
Abstract
Classical 'one-gene/one-disease' models cannot fully reconcile with the increasingly appreciated prevalence of complicated genotype-to-phenotype associations in human disease. Genes and gene products function not in isolation but as components of intricate networks of macromolecules (DNA, RNA, or proteins) and metabolites linked through biochemical or physical interactions, represented in 'interactome' network models as 'nodes' and 'edges', respectively. Accordingly, mechanistic understanding of human disease will require understanding of how disease-causing mutations affect systems or interactome properties. The study of 'edgetics' uncovers specific loss or gain of interactions (edges) to interpret genotype-to-phenotype relationships. We review how distinct genetic variants, the genotype, lead to distinct phenotypic outcomes, the phenotype, through edgetic perturbations in interactome networks altogether representing the 'edgotype'.
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.