University of Rochester
Department of Biology
River Campus Box 270211
Rochester, New York 14627-0211
Hutchison 434 (office)
Hutchison 425 (lab)
(585) 275-7740 (office)
(585) 275-6637 (lab)
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.
To learn more about our research, please visit our lab website Gorbunova Lab.
- 2012. Replicatively senescent cells are arrested in G1 and G2 phases. Aging, In press
- 2012. SIRT6 rescues senescence-related decline in DNA repair by homologous recombination. Proc. Natl. Acad. Sci. USA, In press
- 2012. SIRT1 as a therapeutic target in inflammaging of the pulmonary disease. Prev Med. 2012, 54 Suppl:S20-8
- 2012. Rad51 promoter targeted gene therapy is effective for in vivo visualization and treatment of cancer. Molecular therapy, 20(2):347-55
- 2011. Adenoviral vector driven by a minimal Rad51 promoter is selective for p53-deficient tumor cells. PLOS One, 6(12):e28714
- 2011. Repairing split ends: SIRT6, mono-ADP ribosylation and DNA repair. Aging, (9):829-35
- 2011. Sirt6 overexpression induces massive apoptosis in cancer cells but not in normal cells. Cell Cycle, http://www.ncbi.nlm.nih.gov/pubmed/15888314:3153-8
SIRT6 promotes DNA repair under stress by mono-ADP-ribosylating PARP1.
*Comment in: Sirtuin 6 and DNA Repair, Guy Riddihough, Science Signaling 21 June 2011: ec177.
*Selected for Faculty of 1000
- 2010. Establishing primary adult fibroblast cultures from rodents. JoVE, 8;(43). pii: 2002. doi: 10.3791/2002
- 2010. Analysis of DNA Double-Strand Break (DSB) Repair in Mammalian Cells. JoVE, Oct 5;(44). pii: 2033. doi: 10.3791/2033
Naked mole-rat cells are hypersensitive to contact inhibition – a clue to extraordinary cancer resistance.
Proc. Natl. Acad. Sci, USA, 106(46):19352-7.**
**Received Cozzarelli Prize for a paper of outstanding scientific excellence and originality published in 2009
**Selected for Faculty of 1000
- 2009. DNA repair by homologous recombination, but not by nonhomologous end joining, is elevated in breast cancer cells. Neoplasia, 11(7):683-691.
- 2009. Coevolution of telomerase activity and body mass in mammals: from mice to beavers. Mech. Aging Dev., 130(1-2):3-9.
- 2008. Use of Rad51 promoter for targeted anticancer therapy. Proc Natl Acad Sci 105(53):20810-5.
- 2008. DNA repair by nonhomologous end joining and homologous recombination during cell cycle in human cells. Cell Cycle 7(18):2902-6.
- 2008. Distinct tumor suppressor mechanisms evolve in rodent species that differ in size and lifespan. Aging Cell 7(6):813-823.
- 2008. Comparison of nonhomologous end joining and homologous recombination in human cells. DNA Repair (Amst) 7(10):1765-71.
- 2008. Rodents for comparative aging studies: from mice to beavers. Age 30(2-3):111-119. (Invited review)
- 2008. Genome-wide demethylation promotes triplet repeat instability independently of homologous recombination. DNA Repair (Amst) 7(2):313-20.
- 2007. Changes in DNA repair during Aging. Nucleic Acids Res. 35(22):7466-74. (Invited review)
- 2007. Changes in the level and distribution of Ku proteins during cellular senescence. DNA Repair (Amst) 6(12):1740-8.
- 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.