The University of Washington Molecular Medicine Training Program (MMTP) educates students to work at the interface of basic science and medicine. We request continued funding to support students in the new interdisciplinary and interdepartmental Molecular Medicine and Mechanisms of Disease (M3D) PhD Program. The mission of the M3D PhD Program is to train students to work at the interface of basic science and medicine, enabling them to carry out translational research that meets the highest standards of scientific rigor and medical significance. M3D PhD Program training is distinguished by: ? A core curriculum that provides a foundation in human physiology, pathology and genetics. ? Emphasis on the significance of thesis research to human health and disease. ? Dual mentorship of PhD research by a basic scientist and a clinician or clinician-scientist. ? Direct contact with clinicians and clinical medicine throughout PhD training. Students completing training have the intellectual tools and the experience in clinical environments to create new, imaginative, and comprehensive solutions to major issues in medicine. Graduates will constitute a new cadre of scientists able to apply cutting-edge experimental strategies to solving important questions in human health and disease; and, conversely, to use insights from human disease processes to solve fundamental biological problems.
The University of Washington Molecular Medicine Training Program educates students to work at the interface of basic science and medicine, by incorporating elements of medical training into PhD studies. Our trainees learn to identify and solve important problems in medical science, and to carry out translational research that meets the highest standards of scientific rigor and medical significance. This will lead to improved diagnosis and treatment of human diseases.
|James, Charlotte A; Yu, Krystle K Q; Gilleron, Martine et al. (2018) CD1b Tetramers Identify T Cells that Recognize Natural and Synthetic Diacylated Sulfoglycolipids from Mycobacterium tuberculosis. Cell Chem Biol 25:392-402.e14|
|Keller, Rachel B; Tran, Thao T; Pyott, Shawna M et al. (2018) Monoallelic and biallelic CREB3L1 variant causes mild and severe osteogenesis imperfecta, respectively. Genet Med 20:411-419|
|Faber, Chelsea L; Matsen, Miles E; Velasco, Kevin R et al. (2018) Distinct Neuronal Projections From the Hypothalamic Ventromedial Nucleus Mediate Glycemic and Behavioral Effects. Diabetes 67:2518-2529|
|Dennis, Daniel G; McKay-Fleisch, Jill; Eitzen, Kaila et al. (2017) Normally lethal amino acid substitutions suppress an ultramutator DNA Polymerase ? variant. Sci Rep 7:46535|
|Su, Wei; Aloi, Macarena S; Garden, Gwenn A (2016) MicroRNAs mediating CNS inflammation: Small regulators with powerful potential. Brain Behav Immun 52:1-8|
|Jin, Kelly; Hoffman, Jessica M; Creevy, Kate E et al. (2016) Multiple morbidities in companion dogs: a novel model for investigating age-related disease. Pathobiol Aging Age Relat Dis 6:33276|
|Blakney, Anna K; Little, Adam B; Jiang, Yonghou et al. (2016) In vitro-ex vivo correlations between a cell-laden hydrogel and mucosal tissue for screening composite delivery systems. Drug Deliv 24:582-590|
|Herman, Jacob A; Toledo, Chad M; Olson, James M et al. (2015) Molecular pathways: regulation and targeting of kinetochore-microtubule attachment in cancer. Clin Cancer Res 21:233-9|
|Krishnamurty, Akshay T; Pepper, Marion (2014) Inflammatory interference of memory formation. Trends Immunol 35:355-7|
|Sureka, Kamakshi; Choi, Philip H; Precit, Mimi et al. (2014) The cyclic dinucleotide c-di-AMP is an allosteric regulator of metabolic enzyme function. Cell 158:1389-1401|
Showing the most recent 10 out of 12 publications