Layers of epistasis: genome-wide regulatory networks and network approaches to genome-wide association studies

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Genome-wide Association Studies

Progress in probabilistic generative models has accelerated, developing richer models with neural architectures, implicit densities, and with scalable algorithms for their Bayesian inference. However, there has been limited progress in models that capture causal relationships, for example, how individual genetic factors cause major human diseases. In this work, we focus on two challenges in par...

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Genome-wide Association Studies

Progress in probabilistic generative models has accelerated, developing richer models with neural architectures, implicit densities, and with scalable algorithms for their Bayesian inference. However, there has been limited progress in models that capture causal relationships, for example, how individual genetic factors cause major human diseases. In this work, we focus on two challenges in par...

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Genome-wide association studies.

Genome-wide association (GWA) studies are best understood as an extension of candidate gene association studies, scaled up to cover hundreds of thousands of markers across the genome in samples usually of several thousand cases and controls. The GWA approach allows the detection of much smaller effect sizes than with previous linkage-based genome-wide studies. However, this sensitivity makes th...

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Genome-Wide Association (GWA) Studies

A host of data on genetic variation from the Human Genome and International HapMap projects, and advances in high-throughput genotyping technologies, have made genome-wide association (GWA) studies technically feasible. GWA studies help in the discovery and quantification of the genetic components of disease risks, many of which have not been unveiled before, and have opened a new avenue to und...

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Epistasis Analysis Goes Genome-Wide

Epistasis, a term coined by William Bateson in 1909 [1], refers to the interdependence of mutations in their phenotypic effects. Let the phenotypic value of a trait relative to that of the wild type be fA and fB for mutants A and B, respectively, and let the phenotypic value of the corresponding double mutant be fAB. Although variation exists, epistasis is usually defined by ε = fAB − fAfB and ...

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ژورنال

عنوان ژورنال: Wiley Interdisciplinary Reviews: Systems Biology and Medicine

سال: 2010

ISSN: 1939-5094

DOI: 10.1002/wsbm.132