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

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Publications: __________________________________________________________________________________ Center for Advanced Biotechnology and Medicine Céline Gélinas Luque, I., Zong, W.-X., Chen, C. and Gélinas, C. (2000). N-terminal determinants of IκBα necessary for the cytoplasmic regulation of c-Rel. Oncogene 19: 1239-1244. Chen C., Edelstein, L.C. and Gélinas, C. (2000). Rel/NF-κB directly activates expression of the apoptosis inhibitor Bcl-xL. Mol. Cell. Biol. 20: 2687-2695. Ravi, R., Bedi, G.C., Engstrom, L.W., Zeng, Q., Mookerjee, B., Gélinas, C., Fuchs, E.J. and Bedi, A. (2001) Regulation of death receptor expression and TRAIL/Apo2L-induced apoptosis by NF-κB. Nature Cell Biol. 3: 409-416. Shah, N., Thomas, T.J., Lewis, J.S., Klinge, C.M., Shirahata, A., Gélinas, C. and Thomas, T. (2001). Regulation of estrogenic and nuclear factor κB functions by polyamines and their role in polyamine analog-induced apoptosis of breast cancer cells. Oncogene 20: 1715-1729. 12
Fang Liu, Ph.D. Resident Faculty Member, CABM; Assistant Professor, Rutgers University, Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy Growth and Differentiation Control Laboratory Dr. Fang Liu obtained her B.S. in biochemistry from Beijing University and Ph.D. in biochemistry from Harvard University working with Dr. Michael R. Green. She conducted postdoctoral research with Dr. Joan Massagué at Memorial Sloan-Kettering Cancer Center and joined CABM in 1998. Dr. Liu has received awards from the American Association for Cancer Research-National Foundation for Cancer Research, the Pharmaceutical Research and Manufacturers of America Foundation, the Burroughs Wellcome Fund, and the Sidney Kimmel Foundation for Cancer Research. She also obtained fellowships from the K.C. Wong Education Foundation and the Jane Coffin Childs Memorial Fund for Medical Research. Inhibition of SMAD Transcriptional Activity by Cyclin-Dependent Kinase Phosphorylation: TGF-ß is the most relevant physiological inhibitor of cell proliferation of a wide variety of cell types. During the earliest stage of tumorigenesis, the ability of TGF-ß to inhibit cell growth enables it to act as a potent tumor suppressor. TGF-ß inhibits cell proliferation by causing cell cycle arrest at the G1 phase. SMAD proteins are candidate tumor suppressors and can mediate the TGF-ß growth-inhibitory effects by regulating the expression of several cell cycle-related genes. We have recently discovered that certain SMAD proteins are major substrates for cyclin-dependent kinases (CDKs). We expect that our findings will have a major impact in the cancer research field and may be useful for therapeutic applications. TGF-ß-Inducible Gene Regulation: SMAD proteins can mediate transforming growth factor-ß (TGF-ß) inducible transcriptional responses. In an effort to search for TGF-ß/SMAD inducible genes, we identified Smad7, which is rapidly upregulated by TGF-ß and can antagonize TGF-ß signaling by binding to and inhibiting the TGF-ß receptor function. We found that TGF-ß can stabilize Smad7 mRNA as well as activate Smad7 transcription. The Smad7 promoter is the first TGF-ß responsive promoter identified in vertebrates that contains the 8 base pair palindromic SMAD binding element (SBE), an optimal binding site for SMAD. We are using Smad7 promoter as a model system to elucidate the molecular mechanisms of TGF-ß-inducible gene regulation. We have also identified SMAD interreacting proteins that may regulate SMAD transcription activity and are in the process of characterizing these interacting proteins. Characterization of SMAD4 as a pancreatic tumor suppressor: SMAD4 is a pancreatic tumor suppressor. More than 50% of pancreatic cancers bear mutations in the SMAD4 locus (~30% homozygous deletions and ~22-25% mutations with loss of heterozygosity). The mechanism of how SMAD4 functions as a pancreatic tumor suppressor is not completely defined. Our work is directed towards addressing this important issue. __________________________________________________________________________________ Center for Advanced Biotechnology and Medicine 13
Page 1 and 2: C A B M Center for Advanced Biotech
Page 3 and 4: Director’s Overview The community
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