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Daniel DiMaio

 

Molecular Cell Biology, Genetics & Development; Microbiology

Waldemar Von Zedtwitz Professor of Genetics
Professor of Therapeutic Radiology and Molecular Biophysics & Biochemistry

Education

B.S. Yale University 1974
M.D. Johns Hopkins University 1978
Ph.D. Johns Hopkins University 1981

Research Interests

We use tumor viruses to study the molecular basis of cell proliferation and senescence. We showed that the 44-amino acid transmembrane E5 protein of bovine papillomavirus transforms cells by binding to and activating the platelet-derived growth factor receptor in a ligand-independent fashion, and we are now using the E5 protein as a scaffold to construct novel small transmembrane proteins that modulate cell phenotype and virus replication by interacting with a variety of transmembrane target proteins. We also showed that repression of the human papillomaviruses oncogenes in cervical carcinoma cells activates endogenous tumor suppressor pathways, resulting in cessation of proliferation and rapid entry into a senescent state. We are studying these dramatic effects on cell behavior to discover new principles of cell cycle control and the genetic basis of cellular aging and to develop novel approaches to manipulate these processes and treat cancer.

Links

• DiMaio Homepage

Recent Publications

• Horner, S. and DiMaio, D. (2007). The DNA binding domain of a papillomavirus E2 protein programs a chimeric endonuclease to cleave integrated human papillomavirus DNA in HeLa cervical carcinoma cells. J. Virol. 81 (In press).
• Johung, K., Goodwin. E., and DiMaio, D. (2007). Human papillomavirus E7 repression in cervical carcinoma cells initiates a transcriptional cascade driven by the retinoblastoma family resulting in senescence. J. Virol. 81:2102-2116.

Contact

E-mail
daniel.dimaio@yale.edu