Mingyu Ding Professor of Microbiology and Immunology
Office Phone: 318-675-5760
Laboratory Phone: 318-675-5761
Office Fax: 318-675-5764
Postdoctoral Study, University of Rochester
Ph.D., Molecular Genetics, 1987 University of Konstanz
M.S. (Diplom), Molecular Genetics, 1984, University of Konstanz
B.S. (Vordiplom), Biology, 1981, University of Konstanz
Virus cell interactions, molecular pathogenesis of oncogenic human papillomaviruses
Certain types of human papillomaviruses (HPV) are the major cause of virus-induced malignancies in the human, like cervical carcinoma, the second most common cancer in women worldwide. Papillomaviruses are non-enveloped DNA viruses which exclusively replicate in the skin and mucosa. Due to the dependence on terminally differentiating tissues for their propagation, the study of the papillomavirus life cycle has been hampered. The development of surrogate systems for the generation of papillomaviruses in recent years has now opened ways to investigate processes involved in virus binding, uptake, and intracellular transport as well as the assembly of progeny virus. We are specifically interested in identifying cellular factors functioning as papillomavirus receptors, in the study of virus uptake and intracellular transport, in the analysis of the uncoating process, and the passing of cellular membranes by the virus genome. In addition, we are also studying innate immune defences employed by the host cells to fight off HPV infection.
Dasgupta J, Bienkowska-Haba M, Ortega ME, Patel HD, Bodevin S, Spillmann D, Bishop B, Sapp M, Chen XS. (2011) Structural basis of oligosaccharide receptor recognition by human Papillomavirus. J Biol Chem. Jan 28. 286(4):2617-24. Epub 2010 Nov 29.
Bienkowska-Haba, M. and Sapp, M. (2011): The cytoskeleton in papillomavirus infection. Viruses 3(3):260-271.
Bienkowska-Haba, M., Williams, C., Kim, S.-M., Garcea, R.L., and Sapp, M. (2012): Cyclophilins facilitate dissociation of the HPV16 capsid protein L1 from the L2/DNA complex following virus entry. J. Virol. 86:9875-87. IF: 5.308
Florin, L., Sapp, M., and Spoden, G. (2012): Host cell factors involved in papillomavirus entry. Med Microbiol Immunol 201:437-48.
Spoden, G., Kuhling, L., Cordes, N., Frenzel, B., Sapp, M., Boller, K., Florin, L., Schelhaas, M. (2013): The human papillomaviruses type 16, 18, and 31 share similar endocytic requirements for entry. J Virol 87:7765-73.
Sapp, M.J. (2013) HPV virions hitchhike a ride on retromer complexes. Proc. Natl. Acad. Sci. USA 110:7116-7.
Richards, K.F., Bienkowska-Haba, M., Dasgupta, J., Chen, X. S., and Sapp, M. (2013): Multiple heparan sulfate binding site engagements are required for the infectious entry of human papillomavirus type 16. J Virol 87:11426-37.
DiGiuseppe, S., Bienkowska-Haba, M., Hilbig, L., and Sapp, M. (2014): The nuclear retention signal of HPV16 L2 protein is essential for incoming viral genome to transverse the trans-Golgi network. Virology 458-459:93-105.
Richards, K.F., Mukherjee, S., Bienkowska-Haba, M., Pang, J., and Sapp, M. (2014): Human papillomavirus species-specific interaction with the basement membrane-resident non-heparan sulfate receptor. Viruses 6(12):4856-79.
DiGiuseppe, S., Keiffer, T., Bienkowska-Haba, M., Luszczek, W., Guion, L.G.M., and Sapp, M. (2015): The topography of HPV16 L2 protein in intracellular membranes following infectious entry. J Virol 89: 10442-52.
All Publications: PubMed