Vera Gorbunova
Assistant Professor
Contact Information:
University of Rochester
Department of Biology
River Campus Box 270211
Rochester,
New York 14627-0211
Hutchison 326A
vgorbuno@mail.rochester.edu
585-275-7740
Research Overview
Gorbunova Lab Website
Our research is focused on Aging, DNA repair, and Cancer.
Aging is one of the biggest mysteries of biology. "Why we age?" is a basic biological question, and at the same time it is highly medically relevant. Aging is associated in accumulation of mutations and genomic instability. We study age-related changes in repair of DNA double-strand breaks using human cells and transgenic mice. We are also using comparative approach to study aging by analyzing short- and long-lived animal species. Finally, as aging is associated with increased cancer incidence, we study DNA repair in breast cancer cells, and anti-cancer mechanisms in short- and long-lived rodents.
Publications
- 2007. Changes in DNA repair during Aging. Nucleic Acids Res. In press. (Invited review)
- 2007. Changes in the level and distribution of Ku proteins during cellular senescence. DNA Repair (Amst), In press.
- 2007. TRF2 is required for repair of non-telomeric DNA double-strand breaks by homologous recombination. Proc. Natl. Acad. Sci, USA, 104(32):13068-13073.
- 2007. Telomerase Activity Coevolves with Body Mass not Lifespan. Aging Cell 6(1):45-52.
- 2006. Cell divisions are required for L1 retrotransposition. Mol. Cell. Biol., 27(4):1264-1270.
- 2005. Making ends meet in old age: DSB repair and aging. Mech. Aging. Dev 126(6-7):621-628. (Invited Review)
- 2004. DNA repair by nonhomologous end joining becomes less efficient and more error-prone during cellular senescence. Proc. Natl. Acad. Sci, USA 101(20):7624-7629.
- 2004. Genome-wide demethylation destabilizes CTGáCAG trinucleotide repeats in mammalian cells. Human Molecular Genetics 13(23):2979-2989.
- 2003. Telomerase as a growth promoting factor. Cell Cycle 2(6):534-537.
- 2003. Selectable system for monitoring the instability of CTGáCAG triplet repeats in mammalian cells. Mol. Cell Biol. 23(13):4485-4493.
- 2003. Evidence that high telomerase activity may induce a senescent-like growth arrest in normal human fibroblasts. J. Biol. Chem. 278(9):7692-7698.
- 2002. Expression of hTERT protects normal human fibroblasts from stress-induced apoptosis and necrosis but does not prevent stress-induced premature senescence. J. Biol. Chem. 277(41):38540-38549.
- 2002. CLK-1 protein has DNA binding activity specific to OL region of mitochondrial DNA. FEBS Lett. 516(1-3):279-284.
- 2001. Change of the death pathway in senescent human fibroblasts in response to DNA damage is caused by an inability to stabilize p53. Mol. Cell Biol. 21(5):1552-1564.
- 2000. A new hyperrecombinogenic mutant of nicotiana tabacum. Plant J. 24(5):601-11.
- 2000. Analysis of extrachromosomal Ac/Ds transposable elements. Genetics 155(1):349-359.
- 2000. A nuclear protein that binds specifically to several maize transposons is not essential for Ds1 excision. Mol. Gen. Genet. 263(3):492-497.
- 1999. How plants make ends meet: DNA double-strand break repair. Trends Plant Sci. 4(7):263-269.
- 1997. Nonhomologous DNA end joining in plant cells is associated with deletions and filler DNA insertions. Nucleic Acids Res 25:4650-4657.
- 1997. Circularized Ac/Ds transposons: formation, structure and fate. Genetics 145:1161-1169.