Faculty
| Dr. Nilgun Tumer Professor |
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Education
B.A. Chemistry, Agnes Scott College, 1978
Ph.D. Biochemistry, Purdue University, 1982
Research Interests
Major focus of the research in our laboratory is studying the mechanism by which ribosome
inactivating proteins (RIPs) inhibit cellular translation and viral infection. Pokeweed
antiviral protein (PAP), a ribosome inactivating protein from Phytolacca americana
inhibits translation by catalytically removing a specific adenine residue from the large
rRNA of the 60S subunit of eukaryotic ribosomes. In addition to its ribosome inactivating
ability, PAP has potent activity against many plant and animal viruses including HIV. PAP
has been targeted to cancer cells as the cytotoxic moiety of immunotoxins and has shown
significant clinical antileukemic activity. Our research involves understanding the
mechanism of cytotoxicity and antiviral activity of PAP. We have demonstrated that
expression of PAP in transgenic plants leads to broad spectrum virus resistance. We
investigated the mechanism of cytotoxicity of PAP and demonstrated that cytotoxicity is
not solely due to enzymatic activity, but appears to involve different domains of the
protein. We expressed several non-toxic PAP mutants in transgenic plants and demonstrated
that antiviral activity of PAP can be separated from its cytotoxicity. We recently showed
that PAP inhibits frameshifting and retrotransposition of Ty1 in yeast and identified
yeast chromosomal mutants that are resistant to PAP. Our current research focuses on
characterizing these host genes and determining their role in ribosome depurination and
virus resistance.
Recent Publications
O. Zoubenko, K. Hudak and N. E. Tumer (2000). A nontoxic pokeweed
antiviral protein mutant inhibits pathogen infection via a novel salicylic acid-independent pathway. Plant Mol. Biol., 44, 219-229.P. Wang and N. E. Tumer (2000). Virus resistance mediated by ribosome
inactivating proteins. Advances in Virus Research, 55, 325-356.K. Hudak , P. Wang and N. E. Tumer (2000). Pokeweed antiviral protein
inhibits translation of capped RNAs independently of ribosome depurination by acting directly on the RNA template. RNA, 6, 369-380.P. Wang and N. E. Tumer (1999). Pokeweed antiviral protein cleaves
double-stranded supercoiled DNA using the same active-site required to depurinate rRNA. Nuc. Acids. Res. 27, 1900-1905.
K. A. Hudak, J.D. Dinman and N.E. Tumer (1999). Pokeweed antiviral protein
accesses ribosomes by binding to L3. J. Biol.
Chem 274, 3859-3864.
P. Wang, O. Zoubenko and N. E. Tumer (1998). Reduced toxicity and broad
N.E. Tumer, B. Parikh, P. Li and J. Dinman (1998). Pokeweed antiviral protein specifically
inhibits Ty11 directed +1 ribosomal frameshifting and TY1 retrotransposition
in Saccharomyces cerevisiae, J. Virology, 72, 1036-1042. O. Zoubenko, F. Uckun, Y. Hur, Ilan Chet and N.E. Tumer (1997). Pokeweed
antiviral protein activates plant defense pathways independently of salicylic acid and
leads to resistance to fungal infection. Nature/Biotechnology, 15, 992-996. B. Waurzyniak, E. Schneider, N. Tumer, Y. Yanishevski, R. Gunther, L. Chelstrom,
H. Wendorf, D. Myers, J. Irvin, Y. Messinger, O. E, T. Zeren, M.-C. Langlie, W. Evans, and
F. Uckun (1997). In vivo toxicity, pharmacokinetics, and antileukemic activity of TXU
(Anti-CD7)-pokeweed antiviral protein immunotoxin. Clin. Cancer Research, 3,
881-890. S. Smirnov, V. Schulaev, and N.E. Tumer (1997). Expression of pokeweed
antiviral protein in transgenic plants induces virus resistance in grafted wild type
plants independent of salicylic acid accumulation and pathogenesis-related protein
synthesis. Plant Physiology, 114, 1113-1121. N. E. Tumer, D. J. Hwang and Maureen Bonness (1997). C-terminal deletion mutant of
pokeweed antiviral protein inhibits viral infection but does not depurinate host
ribosomes. Pro. Natl. Acad. Sci. USA, 94, 3866-3871.
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