Faculty

Biochemistry and Molecular Genetics Faculty.

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Contact Information

University Of Illinois at Chicago

Dept. Of Biochemistry and

Molecular Genetics

900 S. Ashland (M/C 669)
Chicago, IL 60607
tel: 312-996-7670
fax: 312-413-0353

Dr. Maxim Frolov

mfrolov@uic.edu

Research Interests:

The research in our lab is focused on understanding the molecular mechanisms of the cell cycle regulation and how these mechanisms are utilized in vivo. Many models attribute a central role in cell cycle regulation to a transcriptional factor E2F and Retinoblastoma tumor suppressor protein (pRB). Importantly, the pRB pathway is functionally inactivated in most tumor cells and it is thought that unrestrained activity of E2F drives inappropriate proliferation in tumors. There has been a significant progress in recent years toward the understanding of the biochemical properties of E2F and pRB proteins and the ways they are regulated. However, the mechanisms by which pRB negatively controls cell proliferation in vivo are not fully understood. Genetically, Drosophila provides a relatively simpler system to study the role of E2F, since the corresponding families are smaller. Our lab is carrying out large scale unbiased genetic screens to identify new genes that interface with the E2F/pRB module in vivo and contribute to its regulation during development.


Dr. Maxim Frolov, Assistant Professor Ph.D, Moscow State University, Russia Postdoctoral Fellow University of Missouri-Columbia, Columbia Massachusetts General Hospital, Harvard Medical School, Boston

We are also interested in dissecting functional interactions between the pRB pathway and other tumor suppressor pathways. Particularly, our focus is on the recently identified Hippo tumor suppressor pathway which negatively regulates organ size in flies and mammals. Given the pivotal role of pRB in tumor suppression, an understanding of how the function of the Drosophila homologues dE2F/pRB is regulated will provide crucial clues in understanding the regulation of mammalian cell growth and the ways in which such controls may go awry in human cancer.

Selected Publications:

Frolov, M.V., D.S. Huen, O. Stevaux, D. Dimova, K. Balczarek-Strang, and N.J. Dyson. 2001. Functional antagonism between E2F family members. Genes & Development15: 2146-2160.

Frolov M.V., O. Stevaux, N.S. Moon, D. Dimova, E.J. Kwon, E.J. Morris, and N.J. Dyson. 2003. G1 cyclin-dependent kinases are insufficient to reverse dE2F2-mediated repression. Genes & Development17: 723-728.

Dimova, D., O. Stevaux, M.V. Frolov, and N.J. Dyson. 2003. Cell cycle-dependent and cell cycle-independent control of transcription by the Drosophila E2F/RB pathway. Genes & Development17: 2308-2320.

Frolov, M.V. and N.J. Dyson. 2004. Molecular mechanisms of E2F-dependent activation and pRB-mediated repression. Journal of Cell Science 117: 2173-2181.

Frolov M.V., N.S. Moon, and N.J. Dyson. 2005. DP is needed for normal cell proliferation. Molecular and Cellular Biology. 25: 3027-3039.

Moon N.S., M.V. Frolov, E.J. Kwon, L. Di Stefano, D.K. Dimova, E.J. Morris, B. Taylor-Harding, K. White, and N.J. Dyson. 2005. Drosophila E2F1 has context-specific pro- and antiapoptotic properties during development. Developmental Cell. 9:463-475.

Rasheva, V.I., D. Knight, P. Bozko, K. Marsh, and M.V. Frolov. 2006. Specific role of the SR protein splicing factor B52 in cell cycle control in Drosophila. Molecular and Cellular Biology. 26:3468-3477.

Ambrus, A. M., B. N. Nicolay, V. I. Rasheva, R. Suckling, and M.V. Frolov. 2007. dE2F2-independent rescue of proliferation in cells lacking an activator dE2F1. Molecular and Cellular Biology. 27:8561-8570. Figure from the paper is featured on the cover of Microbiology and Molecular Biology Reviews, 2008, vol. 72.

Nicolay, B. N. and M.V. Frolov. 2008. Context dependent requirement for dE2F during oncogenic proliferation. PLoS Genetics, 4: e1000205. doi:10.1371/journal.pgen.1000205