I am Senior Lectuer in Genomic Medicine at Imperial College Faculty of Medicine and I lead the Integrative Genomics and Medicine Group of the MRC Institute of Clinical Sciences, which is based on the Hammersmith campus of Imperial College London (http://www.csc.mrc.ac.uk/Research/Groups/GMC/IntegrativeGenomicsMedicine/).
Our research focuses on the integration of genomic, phenotypic and genetic resources to identify risk factors and molecular networks for complex traits and disease.
Understanding how complex disease systems operate requires the integration of multiple layers of biological information from DNA to phenotype. In my group, we integrate informatics and multi-dimensional modelling of genomic data to elucidate the regulatory processes underlying complex traits, including metabolic, cardiovascular, inflammatory, neurological and behavioral phenotypes.
In particular, rather than focusing on single disease susceptibility genes, we explore pathways and networks to better predict the consequences of genetic and epigenetic variations on complex disease. We employ systems-genetics approaches, from model organisms to humans, to provide functional annotation of genes in biological processes and reveal the signal of common genetic variation of small effect that is not captured by typical genome wide association studies.
et al., 2019, WWP2 regulates pathological cardiac fibrosis by modulating SMAD2 signaling (vol 10, 3616, 2019), Nature Communications, Vol:10, ISSN:2041-1723
et al., Integrated systems-genetic analyses reveal a network target for delaying glioma progression, Annals of Clinical and Translational Neurology, ISSN:2328-9503
et al., WWP2 regulates pathological cardiac fibrosis by modulating 2 SMAD2 signaling, Nature Communications, ISSN:2041-1723
et al., 2019, miR-15a/-16 inhibit angiogenesis by targeting the Tie2 coding sequence: Therapeutic potential of a miR-15a/16 decoy system in limb ischemia., Molecular Therapy : Nucleic Acids, Vol:17, ISSN:2162-2531, Pages:49-62
et al., 2019, Intrinsic mutant HTT-mediated defects in oligodendroglia cause myelination deficits and behavioral abnormalities in Huntington disease, Proceedings of the National Academy of Sciences of the United States of America, Vol:116, ISSN:0027-8424, Pages:9622-9627