2001 - Center for Advanced Biotechnology and Medicine - Rutgers ...

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Publications: __________________________________________________________________________________ Center for Advanced Biotechnology and Medicine Michael M. Shen Yan, Y.-T., Stein, S. M., Ding, J., Shen, M. M. and Abate-Shen, C. (2000). A novel PF/PN motif inhibits nuclear localization and DNA binding activity of the ESX1 homeoprotein. Mol. Cell. Biol. 20:661-671. Mudgett, J. S., Ding, J., Guh-Siesel, L., Chartrain, N. A., Yang, L., Gopal, S. and Shen, M. M. (2000). Essential role for p38a mitogen-activated protein kinase in placental angiogenesis. Proc. Natl. Acad. Sci. USA 97:10454-10459. Bamford, R. N., Roessler, E., Burdine, R. D., Saplakoglu, U., de la Cruz, J., Splitt, M., Goodship, J. A., Towbin, J., Bowers, P., Ferrero, G. B., Marino, B., Schier, A. F., Shen, M. M., Muenke, M. and Casey, B. (2000) . Loss-of-function mutations in the EGF-CFC gene Cfc1 are associated with human left-right laterality defects. Nature Genet. 26:365-369. Hu, G., Lee, H., Price, S. M., Shen, M. M. and Abate-Shen, C. (2001) . Msx homeobox genes inhibit differentiation through up-regulation of Cyclin D1. Development 128:2373-2384. Kimura, C., Shen, M. M., Takeda, N., Aizawa, S. and Matsuo, I. (2001) . Complementary functions of Otx2 and Cripto in initial patterning of mouse epiblast. Dev. Biol. 128:2373-384. Review articles (peer-reviewed): Schier, A. F. and Shen, M. M. (2000) . Nodal signalling in vertebrate development. Nature 403:385-389. Shen, M. M. and Schier, A. F. (2000). The EGF-CFC gene family in vertebrate development. Trends Genet. 16:303-309. Abate-Shen, C. and Shen, M. M. (2000). Molecular genetics of prostate cancer. Genes Dev. 14:2410-2434. Book chapters/technical articles/reviews: Shen, M. M. (2001). Identification of differentially expressed genes in mouse development using differential display and in situ hybridization. Methods 24:15-27. Cunha, G. R., Donjacour, A. A., Hayward, S. W., Thomson, A. A., Marker, P. C., Abate-Shen, C., Shen, M. M. and Dahiya, R. (2002). Cellular and molecular biology of prostatic development. In: Prostate Cancer: Principles and Practice. Eds. Kantoff, P. W., Carroll, P., D'Amico, A. V. (Lippincott, Williams and Wilkins, Philadelphia), pp. 16-28. 20
Eileen White, Ph.D. Associate Investigator, Howard Hughes Medical Institute; Resident Faculty Member, CABM; Professor, Rutgers, Department of Molecular Biology and Biochemistry Viral Transformation Laboratory Dr. Eileen White transferred her research program to CABM in July 1990 from Cold Spring Harbor Laboratory where she was a staff investigator. She conducted postdoctoral research at the Cold Spring Harbor laboratory as a Damon Runyon – Walter Winchell Fellow, working with Dr. Bruce Stillman. Her work is currently funded by a MERIT Award from NIH and Howard Hughes Medical Institute. Dr. White is a member of the National Cancer Institute Board of Scientific Counselors. The goal of our research program is to examine viral oncogenes and mechanisms of mammalian cell growth. Specifically, the White lab is working to determine the mechanisms by which oncogenes of the DNA tumor virus adenovirus stimulate cell proliferation and inhibit cell death which leads to malignant transformation. We study the mechanisms by which human DNA tumor viruses deregulate cell cycle and apoptosis (programmed cell death) control in the development of cancer and during productive viral infection. Understanding pathways that control cell proliferation and cell death will lead to better treatments for cancer and viral infections. Description of Research The DNA tumor virus adenovirus infects human cells, recruits them into a proliferative state, and borrows elements of the host cell transcription, translation, and DNA replication machinery to reproduce viral proteins and DNA. In rodent cells which are semipermissive for adenovirus infection, cell growth is deregulated but virus replication is ineffective. As the viral infection does not progress to completion, the deregulation of cell growth control produces transformation. The viral genes required for oncogenic transformation are the E1A and E1B oncogenes. Understanding how the products of these viral oncogenes alter cell growth control pathways is important for establishing how cancer develops. Regulation of programmed cell death (apoptosis) by E1A and E1B is necessary for sustaining a productive infection in human cells and is an integral part of the transformation process in rodent cells. The E1A proteins are responsible for initiating a proliferative response, and an indirect consequence of this required function of E1A is the induction of apoptosis. The E1B gene encodes overlapping, redundant functions to suppress apoptosis, the 19K and 55K proteins. Thus, E1A expression and subsequent growth deregulation can occur unimpeded by cell death in the presence of E1B expression. Without inhibition of apoptosis by E1B, transformation of rodent cells is rare, and premature death of the host cell impairs virus yield in productively infected human cells. The human bcl-2 proto-oncogene, which is known to inhibit apoptosis in other systems, will also suppress apoptosis induced by E1A expression and cooperate with E1A to transform primary rodent cells. Thus, inhibition of apoptosis is an important step in the progression of the transformed state. __________________________________________________________________________________ Center for Advanced Biotechnology and Medicine 21
Page 1 and 2: C A B M Center for Advanced Biotech
Page 3 and 4: Director’s Overview The community
Page 5 and 6: Research Programs and Laboratories
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Page 9 and 10: Isaac Edery, Ph.D. Resident Faculty
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