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PULSe Home > Faculty Members A-C > Ourania Andrisani
Ourania M. Andrisani
Current Research Interests:
Research in my laboratory focuses on the role of the transcription factor CREB (cAMP-response-element binding protein) in mechanisms of growth control and cellular differentiation. We have developed two cellular model systems to study these aspects of CREB function.
The first system is based on the interaction of CREB with the oncoprotein pX, encoded by the Hepatitis B virus; pX is implicated, by an unknown mechanism, in the development of hepatocellular carcinoma (HCC) in humans. Our studies demonstrated that pX increases the transcriptional efficacy of CREB and other bZip transcription factors. We are investigating the mechanism of CREB/pX interactions, the clinical relevance of these interactions in development of hepatocellular carcinoma, and the role of CREB in mechanisms of growth control in hepatocytes.
The second model system addresses the role of CREB in neuronal cell differentiation. Employing as our model system primary cultures of Japanese Quail neural crest cells, we are investigating the role of the cAMP signaling network and its interplay with other cellular transduction systems in neuronal cell differentiation.
Selected Publications:
Bilodeau M., Boulineau, T., Hullinger, R.L. and Andrisani, O. (2000) Cyclic AMP signaling functions as a bimodal switch in sympathoadrenal cell development in cultured primary neural crest cells. Mol. Cell. Biol., 20(9):3004-3014.
Lee, S., C. Tarn, Wang, W.-H., Chen, S., Hullinger, R.L. and O. Andrisani. (2002) Hepatitis B virus X protein differentially regulates cell cycle progression in X-transforming vs. non-transforming hepatocyte (AML12) cell lines. J. Biol. Chem., 277:8730-8740.
Wang, W.H., Gregori, G., Hullinger, R.L. and Andrisani, O.M. (2004) Combined and sustained activation of p38 and JNK pathways by Hepatitis B Virus X protein effects apoptosis via Fas/FasL expression Mol. Cell. Biol.,24,10352-10365,2004
Ji, M. and Andrisani, O.M. (2005) The cAMP signaling network represses sympathoadrenal cell development and promotes melanogenesis in neural crest cells. Mol. Cell. Biol., 5134-5145.
Chen, S., Ji, M., Paris, M., Hullinger, R.L. and Andrisani, O.M. (2005) The cAMP pathway Regulates both transcription and activity of homeodomain transcription factor Phox2a required for development of Neural Crest-derived and CNS-derived Catecholaminergic neurons. J. Biol. Chem., 280, 41025-41036.
Benjanirut C., M. Paris, W-H. Wang, S. Hong, K. Kim, R. L. Hullinger and Andrisani O.M. (2006) The cAMP pathway via CREB, in synergy with BMP2, regulates transcription from the mammalian Phox2a promoter via cAMP-response-element binding sites. J. Biol. Chem., 281,2969-2981.
Paris, M., Wang, W-H. , Shin, M-H., Franklin D.S., and Andrisani O.M. (2006) The transcription factor Phox2a coordinates cell cycle exit and catecholaminergic neuron differentiation in CNS-derived and neural crest progenitors via transcriptional induction of p27Kip1. Mol. Cell. Biol., 26:8826-8839.
Wang WH, Hullinger RL, Andrisani OM. Hepatitis B Virus X Protein via the p38MAPK Pathway Induces E2F1 Release and ATR Kinase Activation Mediating p53 Apoptosis. (2008). J Biol Chem. 283:25455-67.
Rakotomalala L, Studach L, Wang WH, Gregori G, Hullinger RL, Andrisani O. (2008). Hepatitis B virus X protein increases the Cdt 1 to geminin ratio inducing DNA re-replication and polyploidy. J Biol Chem, 283: 28729 287240.
Studach L, Rakotomala L, Wang WH, Hullinger RL Cairo S, Buendia MA, Andrisani O. (2009). Polo-like kinase1 inhibition suppresses Hepatitis B virus X protein-induced transformation, in an in vitro model of liver cancer progression. Hepatology, in press
Shin M-H, Mavila N, Wang WH, Alvarez SV, Hall M, Andrisani O. (2009). Time-dependent activation of Phox2a modulates the amplitude and duration of p27Kip1 transcription. Mol Cell Biol, pending
Xiaoming Yang, Hongchang Li, Zinan Zhou, Wen-Horng Wang, Anping Deng, Ourania Andrisani and Xiaoqi Liu (2009) Plk1-mediated Phosphorylation of Topors Regulates p53 Stability. J Biol Chem, in press
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