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Elliot Androphy, M.D.

Elliot AndrophyProfessor, University of Massachusetts Medical School

Faculty Appointment(s) In: Dermatology, Medicine, Molecular Genetics and Microbiology

Other Affiliation(s): Center for AIDS Research, Clinical and Population Health Research, Graduate School of Biomedical Sciences, Immunology       and Virology, Interdisciplinary Graduate Program

Lazare Research Building, Rm 328
364 Plantation Street
Worcester, Massachusetts 01605
Phone: 508-856-6602
E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it

Research Interests

Pathogenesis of papillomavirus infections

The laboratory studies the pathogenesis of papillomavirus infections, which serve as a model to understand how normal human cells are induced toward cancer.  The E6 and E2 projects involve techniques of cell biology and epithelial cell culture, DNA and RNA manipulation, protein chemistry, yeast genetics, and transgenic animal models.  We also study a common form of muscular dystrophy.  These projects are supported by grants from the NIH. 

Mechanism of papillomavirus mediated cell transformation and development of cancer

Papillomaviruses cause warts and cervical cancer, one of the most common malignancies of women in the world.  We are studying how the viral E6 protein transforms and immortalizes human cells and how these relate to activities necessary for viral DNA replication. We are characterizing E6 interacting proteins and, using expression profiling, identifying cellular transcription programs altered by E6.

Regulation of transcription and DNA replication

The E2 protein regulates viral transcription, DNA replication and coordinates viral genome segregation in mitosis. We investigate the cellular factors necessary for these E2 activities.

Structure based drug design

Working with James Baleja Ph.D., a structural biochemist at Tufts Medical School, we use molecular modeling to design novel viral inhibitors.

Genetics and pathogenesis of Spinal Muscular Atrophy (SMA)

SMA is a common form of muscular dystrophy. The deficient protein, SMN, is thought to be involved in biogenesis of mRNA splicing complexes.  We have shown that SMA results from alternative splicing and we seek to define the cellular splicing factors necessary for correct recognition and processing of its mRNA.  High throughput screens seek to identify chemicals and drugs that modulate mRNA processing and restore expression of the SMN protein.

http://www.umassmed.edu/igp/faculty/androphy.cfm