Andrew P. McMahon
University of Southern California
|
Primary Section: 22, Cellular and Developmental Biology Secondary Section: 42, Medical Physiology and Metabolism Membership Type:
Member
(elected 2020)
|
Biosketch
Andrew McMahon is a developmental geneticist known for his work on cell-cell communication, notably Wnt and Hedgehog-mediated, in vertebrate development. McMahon was born in Birkenhead, in the U.K. He graduated in 1978 from St. Peter’s College, Oxford University with a BA in Zoology and received a PhD in mammalian genetics in 1981 from University College London. After postdoctoral research at the California Institute of Technology (1981-1984). McMahon started his independent research at the National Institute for Medical Research, London. From 1988-1993, McMahon was a faculty within the Roche Institute for Molecular Biology, New Jersey. In 1993, McMahon joined the Faculty of Arts and Sciences at Harvard University. In 2012, McMahon's research moved to the University of Southern California where he is the W.M. Keck Provost and University Professor, chair of the Department of Stem Cell Biology and Regenerative Medicine and director of the Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research. In addition to membership of the National Academy of Sciences, McMahon is an elected fellow of the American Association for the Advancement of Science, the American Academy of Arts and Sciences, the European Molecular Biology Organization, and the Royal Society.
Research Interests
Andrew McMahon’s research is focused on development, injury and repair of the mammalian kidney. The long-term research goal is to generate insight enabling therapeutic advancement. By studying signaling processes, and the transcriptional mediators of signaling activity, the group is building a cellular map of mammalian kidney development. The regulatory cell atlas will guide strategies for engineering functional kidney structures and kidney organoid disease models. The kidney has a limited capacity to repair and the repair mechanisms are poorly understood. Mechanistic insight here will aid approaches to augment repair processes following kidney injury and to prevent chronic disease provoking outcomes.
