My research interests focus on the role of the human epigenetic machinery in human homeostasis. Specifically, I am studying fundamental properties of genes encoding for chromatin modifiers, such as their expression patterns, their tolerance to variation, and their links to specific disease phenotypes. Additionally, I am working on Kabuki syndrome, one of the Mendelian disorders of the epigenetic machinery, where my focus is on characterizing the epigenomic aberrations that occur downstream of the genetic defect and give rise to the disorder.
My research interests lie at the intersection of host-pathogen dynamics, genetic epidemiology, and the immune response to infectious diseases. I hope to utilize genomic data at both the host and pathogen level to study human susceptibility or resistance to certain infectious diseases.
My primary research interest is the gene-environment interplay in the developmental origins of disease. I am especially interested in the ways in which epigenetic modifications in the reproductive and prenatal windows are relevant to health outcomes, particularly for neurodevelopmental disorders such as autism spectrum disorder (ASD).
I am interested in the effect of human genetic variation on susceptibility to infectious disease. I am particularly interested in how genes, pathogens, and environment work together to cause environmental enteric dysfunction in children living in low-resource areas.
My research interests focus on autism spectrum disorder, related neurodevelopmental and neuropsychiatric disorders (NDD/NPD), and other complex human disease phenotypes such as coronary artery disease (CAD). Broadly, I’m interested in a richer understanding of the genotype to phenotype spectrum in complex traits and disease. How do common genetic variants coalesce and contribute to phenotypic variation? What is the interplay between genotype and phenotype in driving disease risk for specific subgroups of individuals? What can we learn from understanding the differences between genotype and phenotype with respect to predicting risk for complex disease? To this end, I aim to elucidate the functional role of common, polygenic variation discovered through GWAS of CAD and NDD/NPD by integrating different omics datasets that measure molecular phenotypes including ChIP-Seq, ATAC-Seq, and RNA-Seq, along with polygenic risk scores that capture genotypic risk for these disorders.
My research interest is to understand the genetic contribution on the diversity of the human immune response, with a particular focus on gene regulation. Integrating this functional information into genetic population studies may offers insights into the mechanism of complex diseases.