Maureen E. Murphy, Ph.D.

faculty photo
Wistar Institute Professor of Genetics
Department: Genetics
Graduate Group Affiliations

Contact information
The Wistar Institute
3601 Spruce Street
Room 352
Philadelphia, PA 19104
Office: 215-495-6870
Lab: 215-495-6869
Education:
B.Sc. (Biochemistry)
Rutgers University, New Brunswick, NJ, 1987.
Ph.D. (Molecular Biology (Donna L. George))
University of Pennsylvania, 1993.
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Description of Research Expertise

The Murphy laboratory focuses on two tumor suppressor proteins that are commonly mutated in human cancer, p53 and p14ARF. The p53 and p14ARF proteins regulate the processes of cell death (apoptosis) and survival (autophagy), respectively. Apoptosis (programmed cell death) is what Murphy describes as the cell’s most important defense mechanism against cancer; this process is kept tightly regulated by p53. In contrast, autophagy (literally, the cell ingesting itself in order to subsist) is a critical survival program for tumor cells. Dr. Murphy’s interest in apoptosis and p53 relates to how genetic polymorphisms in the p53 tumor suppressor gene that are more common in African Americans affect the ability of this protein to induce apoptosis and growth arrest, and hence combat tumor development. Her studies have relevance for understanding inter-individual differences in cancer risk and therapy, particularly in ethnic populations where these variants occur with high frequency. With regard to autophagy, Dr. Murphy proposes to target the autophagy pathway for cancer therapy by using small molecule inhibitors of Heat Shock Protein 70 (HSP70) in order to selectively eradicate tumor cells.

Selected Publications

Kung, C. P., Budina, A., Balaburski, G., Bergenstock, M. K., Murphy, M.: Autophagy in tumor suppression and cancer therapy. Critical reviews in eukaryotic gene expression 21(1): 71-100, 2011.

Leu, J. I., Pimkina, J., Pandey, P., Murphy, M. E., George, D. L.: HSP70 inhibition by the small-molecule 2-phenylethynesulfonamide impairs protein clearance pathways in tumor cells. Molecular cancer research : MCR 9(7): 936-47, 2011.

Pimkina, J., Murphy, M. E.: Interaction of the ARF tumor suppressor with cytosolic HSP70 contributes to its autophagy function. Cancer biology & therapy 12(6): 503-9, 2011.

Frank, A. K., Leu, J. I., Zhou, Y., Devarajan, K., Nedelko, T., Klein-Szanto, A., Hollstein, M., Murphy, M. E.: The codon 72 polymorphism of p53 regulates interaction with NF-{kappa}B and transactivation of genes involved in immunity and inflammation. Molecular and cellular biology 31(6): 1201-13, 2011.

Frank, A. K., Pietsch, E. C., Dumont, P., Tao, J., Murphy, M. E.: Wild-type and mutant p53 proteins interact with mitochondrial caspase-3. Cancer biology & therapy 11(8): 740-5, 2011.

Feng, Z., Zhang, C., Kang, H. J., Sun, Y., Wang, H., Naqvi, A., Frank, A. K., Rosenwaks, Z., Murphy, M. E., Levine, A. J., Hu, W.: Regulation of female reproduction by p53 and its family members. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 25(7): 2245-55, 2011.

Azzam, G. A., Frank, A. K., Hollstein, M., Murphy, M. E.: Tissue-specific apoptotic effects of the p53 codon 72 polymorphism in a mouse model. Cell cycle 10(9): 1352-5, 2011.

Whibley, C., Odell, A. F., Nedelko, T., Balaburski, G., Murphy, M., Liu, Z., Stevens, L., Walker, J. H., Routledge, M., Hollstein, M.: Wild-type and Hupki (human p53 knock-in) murine embryonic fibroblasts: p53/ARF pathway disruption in spontaneous escape from senescence. The Journal of biological chemistry 285(15): 11326-35, 2010.

Balaburski, G. M., Hontz, R. D., Murphy, M. E.: p53 and ARF: unexpected players in autophagy. Trends in cell biology 20(6): 363-9, 2010.

Pimkina, J., Humbey, O., Zilfou, J. T., Jarnik, M., Murphy, M. E.: ARF induces autophagy by virtue of interaction with Bcl-xl. The Journal of biological chemistry 284(5): 2803-10, 2009.

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Last updated: 01/28/2014
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