ArticlePLoS computational biology2017
Inferring modulators of genetic interactions with epistatic nested effects models.
Article in PLoS computational biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed.
- Hierarchy of TGFβ/SMAD, Hippo/YAP/TAZ, and Wnt/β-catenin signaling in melanoma phenotype switching.Life science alliance · 2022Article
- Functional network motifs defined through integration of protein-protein and genetic interactions.PeerJ · 2022Article
- Extending the lymphoblastoid cell line model for drug combination pharmacogenomics.Pharmacogenomics · 2021Review
- NEM-Tar: A Probabilistic Graphical Model for Cancer Regulatory Network Inference and Prioritization of Potential Therapeutic Targets From Multi-Omics Data.Frontiers in genetics · 2021Article
- The ability of transcription factors to differentially regulate gene expression is a crucial component of the mechanism underlying inversion, a frequently observed genetic interaction pattern.PLoS computational biology · 2019Article
- Single cell network analysis with a mixture of Nested Effects Models.Bioinformatics (Oxford, England) · 2018Article
- Bioinformatics challenges and perspectives when studying the effect of epigenetic modifications on alternative splicing.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Maps of genetic interactions can dissect functional redundancies in cellular networks. Gene expression profiles as high-dimensional molecular readouts of combinatorial perturbations provide a detailed view of genetic interactions, but can be hard to interpret if different gene sets respond in different ways (called mixed epistasis). Here we test the hypothesis that mixed epistasis between a gene pair can be explained by the action of a third gene that modulates the interaction. We have extended the framework of Nested Effects Models (NEMs), a type of graphical model specifically tailored to analyze high-dimensional gene perturbation data, to incorporate logical functions that describe interactions between regulators on downstream genes and proteins. We benchmark our approach in the controlled setting of a simulation study and show high accuracy in inferring the correct model. In an application to data from deletion mutants of kinases and phosphatases in S. cerevisiae we show that epistatic NEMs can point to modulators of genetic interactions. Our approach is implemented in the R-package 'epiNEM' available from https://github.com/cbg-ethz/epiNEM and https://bioconductor.org/packages/epiNEM/.
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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.