Dr. Sarah Tersey is an islet biologist whose research focuses on the role of the ß-cell in the development of type 1 and type 2 diabetes. The primary goal of her research focuses on understanding the molecular pathways that play a role in the development of diabetes. Specifically, pathways that include the enzymes 12-lipoxygnease and deoxyhypusine synthase. By using inhibitors against these pathways or creating genetic deletions of either of these genes, Dr. Tersey has shown that diabetes can be prevented. A second major focus of her research is the development of biomarkers that will best predict the likelihood of any one individual’s risk to develop type 1 diabetes. Within this concept, she demonstrated that the dysfunction of the pancreatic islet precedes the onset of type 1 diabetes. This research has changed the standard dogma of the islet as a silent bystander to the immune system, to the new way of thinking – that the pancreatic islet is a major player in its own demise during the pre-course of type 1 diabetes.
University of Virgina
Charlottesville, VA
Postdoctoral Fellow - Diabetes and Endocrinology
2008
Massachusetts General Hospital/Harvard Medical School
Boston, MA
Postdoctoral Fellowship - Neuroendocrinology
2007
University of Massachusetts
Amherst, MS
Ph.D. - Animal Biotechnology
2005
Colorado State University
Fort Collins, CO
B.S. - Animal Science
2000
12-Lipoxygenase inhibition suppresses islet immune and inflammatory responses and delays autoimmune diabetes in human gene replacement mice.
12-Lipoxygenase inhibition suppresses islet immune and inflammatory responses and delays autoimmune diabetes in human gene replacement mice. bioRxiv. 2024 Jul 28.
PMID: 39091839
Inhibition of the eukaryotic initiation factor-2a kinase PERK decreases risk of autoimmune diabetes in mice.
Inhibition of the eukaryotic initiation factor-2a kinase PERK decreases risk of autoimmune diabetes in mice. J Clin Invest. 2024 Jun 18; 134(16).
PMID: 38889047
Inhibition of the Eukaryotic Initiation Factor-2-a Kinase PERK Decreases Risk of Autoimmune Diabetes in Mice.
Inhibition of the Eukaryotic Initiation Factor-2-a Kinase PERK Decreases Risk of Autoimmune Diabetes in Mice. bioRxiv. 2024 Jun 03.
PMID: 38895427
Discordant Effects of Polyamine Depletion by DENSpm and DFMO on ß-cell Cytokine Stress and Diabetes Outcomes in Mice.
Discordant Effects of Polyamine Depletion by DENSpm and DFMO on ß-cell Cytokine Stress and Diabetes Outcomes in Mice. Endocrinology. 2024 Jan 16; 165(3).
PMID: 38195178
Leukotriene B4 receptor 2 governs macrophage migration during tissue inflammation.
Leukotriene B4 receptor 2 governs macrophage migration during tissue inflammation. J Biol Chem. 2024 Jan; 300(1):105561.
PMID: 38097183
Inhibition of polyamine biosynthesis preserves ß cell function in type 1 diabetes.
Inhibition of polyamine biosynthesis preserves ß cell function in type 1 diabetes. Cell Rep Med. 2023 11 21; 4(11):101261.
PMID: 37918404
Protocol to isolate immune cells from mouse pancreatic lymph nodes and whole pancreas for mass cytometric analyses.
Protocol to isolate immune cells from mouse pancreatic lymph nodes and whole pancreas for mass cytometric analyses. STAR Protoc. 2023 03 17; 4(1):101938.
PMID: 36520629
Inside the ß Cell: Molecular Stress Response Pathways in Diabetes Pathogenesis.
Inside the ß Cell: Molecular Stress Response Pathways in Diabetes Pathogenesis. Endocrinology. 2022 11 14; 164(1).
PMID: 36317483
Identification of a naturally-occurring canine model for early detection and intervention research in high grade urothelial carcinoma.
Identification of a naturally-occurring canine model for early detection and intervention research in high grade urothelial carcinoma. Front Oncol. 2022; 12:1011969.
PMID: 36439482
Proinflammatory signaling in islet ß cells propagates invasion of pathogenic immune cells in autoimmune diabetes.
Proinflammatory signaling in islet ß cells propagates invasion of pathogenic immune cells in autoimmune diabetes. Cell Rep. 2022 06 28; 39(13):111011.
PMID: 35767947