Department of Cell Biology

The Department of Cell Biology pursues fundamental discoveries about how changes in cell growth, survival and function underlie human diseases and identifies new strategies that could contribute to improved quality of life. A central theme in all department work is exploring how tissue-specific stem cells are regulated to maintain physiological homeostasis in tissues and how inappropriate growth of cells with these characteristics causes tumorigenesis.

The proper regulation of cellular division, differentiation and survival is required for all development in multi-cellular organisms, and the dysregulation of these processes causes all human disease. The Department of Cell Biology focuses on discovering the mechanisms that underlie these processes, with a goal of understanding both how they normally occur and how alterations in these processes cause human disease. To this end, laboratories in the department investigate the molecular mechanisms that control cellular processes such as proliferation, apoptosis (programmed cell death), senescence (cellular aging), signal transduction (how cells respond to signals from their environment), and differentiation (how cells change characteristics).


Recent Publications

Liu Y, Molchanov V, Yang T. 2021. Enzymatic machinery of ubiquitin and ubiquitin-like modification systems in chondrocyte homeostasis and osteoarthritis. Curr Rheumatol Rep 23:62.

Zhong ZA, Michalski, MN, Stevens PD, Sall EA, Williams BO. 2021. Regulation of Wnt receptor activity: Implications for therapeutic development in colon cancer. J Biol Chem:100782.

McDowell CT, Klamer Z, Hall J, West CA, Wisniewski L, Powers TW, Angel P, Mehta AS, Lewin DN, Haab BB, Drake R. 2020. Imaging mass spectrometry and lectin analysis of N-linked glycans in carbohydrate antigen defined pancreatic cancer tissues. Mol Cell Proteomics 20:100012.
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Grit JL, Johnson BK, Dischinger PS, Essenburg CJ, Adams M, Campbell S, Pollard K, Pratilas CA, Triche TJ Jr., Graveel CR, Steensma MR. 2021. Distinctive epigenomic alterations in NF1-deficient cutaneous and plexiform neurofibromas drive differential MKK/p38 signaling. Epi Chromatin 14(7).