Geoffrey M. Cooper
Professor of Biology and
Associate Dean of the Faculty, Natural Sciences
PhD, University of Miami, 1973
Areas of interest: cancer, programmed cell death, signal transduction, gene expression
Our laboratory studies the roles of proto-oncogene proteins in the signal transduction pathways that control proliferation, survival and differentiation of mammalian cells. Current research is focused on 1) the mechanisms by which the phosphatidylinositol 3-kinase (PI 3-kinase)/Akt signaling pathway regulates cell survival by suppressing apoptosis and 2) the mechanism by which the MEK/ERK pathway acts to induce neuronal differntiation.
The effects of these signaling pathways are mediated in large part by changes in gene expression, and our studies have focused on using global gene expression profiling to identify the genes that are regulated by PI 3-kinase/Akt signaling and MEK/ERK signaling associated with cell survival and differentiation, respectively. We have combined these results with computational prediction of transcription factor binding sites to identify transcription factors that are targeted by these pathways, and thus to infer the gene regulatory networks that mediate these cellular responses. Ongoing studies are focused on understanding the gene regulatory networks controlled by these pathways in a variety of different types of mammalian cells, including human cancer cells with varying oncogene mutations, neuronal cells and embryonic cells.
- BI 203 Cell Biology
- BI 213 Honors Cell Biology
- Nayak G, Cooper GM. (2012). p53 is a major component of the transcriptional and apoptotic program regulated by PI 3-kinase/Akt/GSK3 signaling. Cell Death Dis. 3:e400.
- Tullai JW, Tacheva S, Owens LJ, Graham JR, Cooper GM. (2011). AP-1 is a component of the transcriptional network regulated by GSK-3 in quiescent cells. PLoS ONE 6:e20150.
- Terragni J, Nayak, G, Banerjee S, Medrano JL, Graham JR, Brennan JF, Sepulveda S, Cooper GM. (2011). The E-Box binding factors Max/Mnt, MITF and USF1 Act coordinately with FoxO to regulate expression of Pro-apoptotic and cell cycle control genes by phosphatidylinositol 3-kinase/Akt/GSK3 signaling. J. Biol. Chem. 286: 36215-36227.
- Mullenbrock S, Shah J, Cooper GM. (2011). Global expression analysis identified a preferentially nerve growth factor-induced transcriptional program regulated by sustained mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) and AP-1 activation during PC12 differentiation. J. Biol. Chem. 286:45131-45145.
- Graham, J.R., Hendershott, M.C., Terragni, J. and Cooper, G.M. (2010). mRNA degradation plays a significant role in the program of gene expression regulated by phosphatidylinositol 3-kinase signaling. Mol. Cell. Biol. 30: 5295-5305.
- Graham JR, Tullai JR and Cooper GM. (2010). GSK-3 represses growth factor-inducible genes by inhibiting NF-kB in quiescent cells. J. Biol. Chem. 285: 4472-4480.
- Terragni J, Graham, JR, Adams KW, Schaffer MW, Tullai JW, Cooper GM. (2008). Phosphatidylinositol 3-kinase signaling in proliferating cells maintains an anti-apoptotic transcriptional program mediated by inhibition of FOXO and non-canonical activation of NFkB transcription factors. BMC Cell Biol. 9, 6.
- Tullai JW, Schaffer ME, Mullenbrock S, Sholder G, Kasif S, Cooper GM. (2007). Immediate-early and delayed primary response genes are distinct in function and genomic architecture. J. Biol. Chem. 282, 23981-23995.