Amy N. Abell
Assistant Professor
Department of Biological Sciences
The University of Memphis
United States of America
Biography
Dr. Abell joined the Department in 2013. She teaches BIOL4094 Biology of Stem Cells and BIOL7730/8730 Stem Cells: Culture/Appl. She began her research career as graduate student studying the structure and function of G protein coupled receptors that are essential for reproduction. During her post-doctoral training, she created a mouse model with neural tube, skeletal and implantation defects. These defects are all related to perturbations in epithelial to mesenchymal transition (EMT), a biological process controlling the conversion of stationary epithelial stem cells to motile mesenchymal cells. Importantly, EMT is essential for normal development, but it is reactivated in several pathologies including organ fibrosis and cancer metastasis. Dr. Abell's lab uses stem cells that she has isolated from mice with EMT related defects to define the signaling/gene expression networks regulating EMT. One goal of her research is to identify novel master regulators of EMT and the reverse process MET. This information will be used in designing new strategies for regenerative medicine and the treatment of EMT related pathologies. Projects in the lab use molecular, cellular and embryological tools to identify regulators of EMT.
Research Interest
Epithelial to mesenchymal transition (EMT), a biological program that is critical during development and is reactivated during organ fibrosis and cancer metastasis, Epithelial stem cells and their transition to mesenchymal cells through EMT, EMT in breast cancer metastasis, EMT during placentation and embryonic development, Epigenetic mechanisms that regulate gene expression important for EMT in stem cells and in cancer.
Publications
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Midland, A.A., Whittle, M.C., Duncan, J.S., Abell, A.N., Nakamura, K., Zawistowski, J.S., Carey, L.A., Earp, H.S., Graves, L.M., Gomez, S.M., and Johnson, G.L., (2012). Defining the expressed breast cancer kinome. Cell Research 22, 620-623.
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Duncan, J.S., Whittle, M.C., Nakamura, K., Abell, A.N., Midland, A.A., Zawistowski, J.S., Johnson, N.L., Granger, D.A., Jordan, N.V., Darr, D.B., Usary, J., Kuan, P.F., Smalley, D.M., Major, B., He, X., Hoadley, K.A., Zhou, B., Sharpless, N.E., Perou, C.M., Kim, W.Y., Gomez, S.M., Chen, X., Jin, J., Frye, S.V., Earp, H.S., Graves, L.M., and Johnson, G.L., (2012). Dynamic reprogramming of the kinome in response to targeted MEK inhibition in triple negative breast cancer. Cell 149, 307-321.
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Jordan, N.V., Prat, A., Abell, A.N., Sciaky, N., Karginova, O.A., Zhou, B., Golitz, B.T., Perou, C.M., and Johnson, G.L., (2013). SWI/SNF chromatin-remodeling factor Smarcd3/Baf60c controls EMT by inducing non-canonical Wnt5a signaling. Mol Cell Biol. 33, 3011-3025.
