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

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__________________________________________________________________________________ Center for Advanced Biotechnology and Medicine Isaac Edery understanding how the daily changes in visible light modulate the oscillatory mechanism. In addition, we recently showed that the splicing efficiency of an intron in the 3' untranslated region of per is thermosensitive. At lower temperatures this intron is spliced more efficiently leading to higher levels of per mRNA and mainly daytime activity. By regulating the splicing efficiency of this intron flies are active during the warmer daytime hours during autumn/winter days typical of temperate zones and avoid the midday sun by manifesting mainly nocturnal activity during the warmer spring/summer seasons. We are continuing these studies to understand how a clock helps measure calendar time by adapting to seasonal changes in temperature and daylength. Given the similarities in the circadian timing mechanisms operating in Drosophila and mammals, we anticipate that our findings will continue to provide important insights into disorders associated with clock malfunction in humans, including manic-depression, seasonal affective disorders (SAD or winter depression), chronic sleep problems in the elderly and symptoms associated with transmeridian flight ("jet-lag") and shift-work. Publications: Bae, K., Lee, C., Hardin, P.H. and Edery, I. (2000). dCLOCK is present in limiting amounts and likely mediates daily interactions between the dCLOCK-CYC transcription factor and the PER-TIM complex. J. of Neurosci. 20, 1746-1753. Edery, I. (2000). Circadian rhythms in a nutshell. Physiol. Genomics 3, 59-74. Kim, E.Y., Bae, K., Ng, F.S., Glossop, N.R.J., Hardin, P.E. and Edery, I. Drosophila CLOCK protein is under posttranscriptional control and influences light-induced activity. Neuron. In press. 10
Céline Gélinas, Ph.D. Resident Faculty Member, CABM; Professor, UMDNJ-Robert Wood Johnson Medical School, Department of Biochemistry Tumor Virology Laboratory Dr. Céline Gélinas came to CABM in September 1988 from the University of Wisconsin where she conducted postdoctoral studies with Nobel laureate Dr. Howard M. Temin. She earned her Ph.D.at the Université de Sherbrooke in her native country, Canada, and received a number of honors including the Jean-Marie Beauregard Award for Academic and Research Excellence and the National Cancer Institute of Canada King George V Postdoctoral Fellowship. Her work is currently funded by the NIH and The Cure for Lymphoma Foundation. Our laboratory has a long-standing interest in the role of the Rel/NF-κB proteins in the onset and progression of hematopoietic and solid tumors. Proteins in the Rel/NF-κB-family of transcription factors play fundamental roles in immune and inflammatory responses, and are implicated in the control of cell proliferation, the inhibition of apoptosis and in oncogenesis. Experimental evidence linking deregulated Rel/NF-κB activity to human cancer has emerged in recent years, consistent with the acute oncogenicity of the Rel/NF-κB oncoprotein v-Rel in inducing fatal leukemia/lymphomas in animal models. Aberrant Rel/NF-κB activity is found in various human leukemias, lymphomas, myelomas and Hodgkin’s disease. Chromosomal amplification, rearrangement, overexpression and/or constitutive activation of the rel and nf-κB genes are also observed in breast, colon, lung, ovarian and prostate cancer. The viral and cellular Rel proteins offer a powerful system to study how the Rel/NF-κB factors function in normal lymphoid cells and to understand how their aberrant activities lead to cancer. Our research focuses on the transcriptional activity and regulation of the Rel/NF-κB factors, on their role in cell growth, apoptosis and oncogenesis, and on the cellular genes that they control. In prior studies, we demonstrated that the transcriptional and anti-apoptotic activities of the v-Rel oncoprotein were necessary for its oncogenic function. Our analyses characterizing Rel-mediated effects on cell survival and neoplasia have recently demonstrated the ability of a subset of mammalian cellular Rel/NF-κB factors to malignantly transform primary lymphoid cells. Detailed analyses of the determinants required for this activity are starting to provide important insights into the mechanisms involved in tumors associated with aberrant Rel/NF-kB function. Our recent experiments suggest that the specificity of target gene activation is likely to play a critical role in the oncogenic conversion of cellular Rel/NF-kB factors. Our ongoing functional characterization of the Rel/NF-kB target genes Bfl-1/A1 and TAPIR and the analysis of their transcriptional regulation by Rel/NF-κB offers new avenues to characterize the Rel/NF-kB signaling pathway and its role in cell survival. This comprehensive approach will help to clarify the mechanism by which Rel/NF-κB proteins function in the immune system and in oncogenesis. In addition, since Rel/NF-κB activity has been implicated in various disease conditions, the systematic analysis of Rel/NF-κB regulation and relevant Rel/NF-κB target genes may also provide important insights into novel approaches for therapeutic intervention. __________________________________________________________________________________ Center for Advanced Biotechnology and Medicine 11
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
Page 7 and 8: Cory Abate-Shen, Ph.D. Resident Fac
Page 9: Isaac Edery, Ph.D. Resident Faculty
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Page 15 and 16: Peter Lobel, Ph.D. Resident Faculty
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Page 19 and 20: Michael M. Shen, Ph.D. Resident Fac
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Page 41 and 42: Aaron J. Shatkin, Ph.D. Director, C
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Page 45 and 46: January 24 James Manley, Biological
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