Ingrid K. Ruf
Molecular Biology & Biochemistry
School of Biological Sciences
Phone: (949) 824-4485
Email: iruf@uci.edu
http://www.faculty.uci.edu/profile.cfm?faculty_id=4945
Ingrid Ruf
Epstein-Barr virus (EBV) encodes a bona fide oncoprotein which contributes to tumorigenicity in several EBV-associated malignancies. However, the contribution of EBV to Burkitt lymphoma (BL) is less clear as this oncoprotein is not expressed in BL tumors or tumor-derived cell lines. Dr. Ruf’s previous work has demonstrated that loss of the EBV genome from a BL-derived cell line resulted in a concomitant loss of tumorigenic potential in a SCID mouse model. Re-infection of these cells with EBV restored full tumorigenic potential to these cells, thereby supporting a direct contribution of the virus to tumor formation. Their more recent work has focused on two small non-coding viral RNAs (EBERs) which are highly expressed in cells maintaining a latent EBV infection. They have shown that these RNAs enhance tumorigenic potential in their BL model and that they promote resistance to interferon-alpha-induced apoptosis. Current research is focused on defining potential mechanisms of actions for the EBERs. Specifically, they are investigating the signal transduction pathways utilized in the inhibition of interferon-induced apoptosis, defining cellular interaction partners of the EBERs (both protein and RNA), characterizing changes in protein expression in EBER-expressing cells, and pursuing the hypothesis that through interaction with specific cellular proteins the EBERs may alter internal ribosome entry site (IRES)-mediated translation. As contributors to both enhanced cell growth potential and decreased cell death, the EBERs are likely to play a key role in EBV-associated cancers.
Selected Publications:
Ruf, I. K., Moghaddam, A., Wang, F., and Sample, J. (1999). Mechanisms that regulate Epstein-Barr virus EBNA-1 gene transcription during restricted latency are conserved among lymphocryptoviruses of Old World primates. J Virol 73(3), 1980-9.
Ruf, I. K., Rhyne, P. W., Yang, H., Borza, C. M., Hutt-Fletcher, L. M., Cleveland, J. L., and Sample, J. T. (1999). Epstein-barr virus regulates c-MYC, apoptosis, and tumorigenicity in Burkitt lymphoma. Mol Cell Biol 19(3), 1651-60.
Swart, R., Ruf, I. K., Sample, J., and Longnecker, R. (2000). Latent membrane protein 2A-mediated effects on the phosphatidylinositol 3-Kinase/Akt pathway. J Virol 74(22), 10838-45.
Ruf, I. K., Rhyne, P. W., Yang, C., Cleveland, J. L., and Sample, J. T. (2000). Epstein-Barr virus small RNAs potentiate tumorigenicity of Burkitt lymphoma cells independently of an effect on apoptosis. J Virol 74(21), 10223-8.
Ruf, I. K., Lackey, K. A., Warudkar, S., and Sample, J. T. (2005). Protection from interferon-induced apoptosis by Epstein-Barr virus small RNAs is not mediated by inhibition of PKR. J Virol 79(23), 14562-9. |
