Kelly Ten Hagen, Ph.D. (original) (raw)

Research Interests

Cells of the body are decorated with a variety of carbohydrates (sugars) that serve diverse functions. Alterations in the presence of these sugars are associated with a number of human diseases, including familial tumoral calcinosis and various cancers. To better understand how alterations in glycosylation contribute to disease onset and progression, Dr. Ten Hagen’s group studies how sugar addition (O-glycosylation) is regulated and how it influences basic biological processes. Using Drosophila models, the group has demonstrated that O-glycosylation is an essential modification that is required in specific cells and tissues during development. Current research is directed at further defining the role this protein modification plays in secretion, secretory vesicle formation, cell adhesion, and cell signaling in both Drosophila and mammals. Ultimately, the aim is to elucidate how O-glycosylation regulates key cellular processes during development and disease.

Dr. Kelly Ten Hagen received a B.S. from Cornell University (with distinction and honors) and earned a Ph.D. in genetics at Stanford University. Dr. Ten Hagen is an elected Fellow of the American Association for the Advancement of Science (AAAS) and the American Society for Biochemistry and Molecular Biology (ASBMB). She received the Rosalind Kornfeld Award for Lifetime Achievement in Glycobiology and was selected for the Irwin J. Goldstein Lectureship. Dr. Ten Hagen has served as an editorial board member for The Journal of Biological Chemistry and for Glycobiology. She was a member of the Board of Directors for the Society for Glycobiology and served as a Council Member for the ASBMB. She is currently on the Board of Reviewing Editors for eLife. She has previously served on the NIH Central Tenure Committee and the NIH Board of Scientific Directors. Dr. Ten Hagen’s research advances our understanding of the molecular, cellular and organismal impact of protein glycosylation and how aberrations in this conserved modification lead to disease.