Vera Gorbunova

Summary

Affiliation: University of Rochester
Country: USA

Publications

  1. ncbi Expression of human telomerase (hTERT) does not prevent stress-induced senescence in normal human fibroblasts but protects the cells from stress-induced apoptosis and necrosis
    Vera Gorbunova
    Huffington Center on Aging, Baylor College of Medicine, Houston, Texas 77030, USA
    J Biol Chem 277:38540-9. 2002
  2. ncbi Changes in DNA repair during aging
    Vera Gorbunova
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Nucleic Acids Res 35:7466-74. 2007
  3. ncbi Making ends meet in old age: DSB repair and aging
    Vera Gorbunova
    Department of Biology, University of Rochester, NY 14627, USA
    Mech Ageing Dev 126:621-8. 2005
  4. ncbi Distinct tumor suppressor mechanisms evolve in rodent species that differ in size and lifespan
    Andrei Seluanov
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Aging Cell 7:813-23. 2008
  5. ncbi Sirtuin 6 (SIRT6) rescues the decline of homologous recombination repair during replicative senescence
    Zhiyong Mao
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Proc Natl Acad Sci U S A 109:11800-5. 2012
  6. ncbi Hypersensitivity to contact inhibition provides a clue to cancer resistance of naked mole-rat
    Andrei Seluanov
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Proc Natl Acad Sci U S A 106:19352-7. 2009
  7. ncbi Replicatively senescent cells are arrested in G1 and G2 phases
    Zhiyong Mao
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Aging (Albany NY) 4:431-5. 2012
  8. ncbi SIRT6 overexpression induces massive apoptosis in cancer cells but not in normal cells
    Michael Van Meter
    University of Rochester, Rochester, NY, USA
    Cell Cycle 10:3153-8. 2011
  9. ncbi Repairing split ends: SIRT6, mono-ADP ribosylation and DNA repair
    Michael Van Meter
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Aging (Albany NY) 3:829-35. 2011
  10. ncbi Cancer resistance in the blind mole rat is mediated by concerted necrotic cell death mechanism
    Vera Gorbunova
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Proc Natl Acad Sci U S A 109:19392-6. 2012

Research Grants

  1. Molecular mechanism of age-related decline of nonhomologous DNA end joining
    Vera Gorbunova; Fiscal Year: 2007
  2. Comparative Analysis of DNA Break Repair in Short- and Long-Lived Rodent Species
    Vera Gorbunova; Fiscal Year: 2010
  3. Molecular mechanism of age-related decline of nonhomologous DNA end joining
    Vera Gorbunova; Fiscal Year: 2010

Collaborators

  • K C Catania
  • DAVEN PRESGRAVES
  • Ying Jiang
  • Eviatar Nevo
  • Andrei V Gudkov
  • Irfan Rahman
  • Andrei Seluanov
  • Zhiyong Mao
  • Michael Van Meter
  • Christopher Hine
  • Christopher M Hine
  • Michael Bozzella
  • Xiao Tian
  • Vincent Fong
  • Vincent Dion
  • Tais H C Sasahara
  • Antonio A C M Ribeiro
  • Xi Shi
  • John H Wilson
  • Zhongle Ke
  • Zhonghe Ke
  • Amita Vaidya
  • Stephen Dewhurst
  • Yo El Kim
  • Cristina Capella
  • Marika Osterbur
  • Matthew Au
  • Marina Feigenson
  • Xiang Liu
  • Jorge Azpurua
  • Yunfu Lin
  • Sharyl L Fyffe
  • Amelia Hall
  • Brandee A Price
  • Jacquelynn Danek
  • Zhuoxun Chen
  • Nola Hause
  • Olivia M Pereira-Smith
  • David Mittelman

Detail Information

Publications29

  1. ncbi Expression of human telomerase (hTERT) does not prevent stress-induced senescence in normal human fibroblasts but protects the cells from stress-induced apoptosis and necrosis
    Vera Gorbunova
    Huffington Center on Aging, Baylor College of Medicine, Houston, Texas 77030, USA
    J Biol Chem 277:38540-9. 2002
    ..We hypothesize that healing of DNA breaks by telomerase inhibits the induction of cell death, but because healing does not provide legitimate DNA repair, it does not protect cells from SIPS...
  2. ncbi Changes in DNA repair during aging
    Vera Gorbunova
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Nucleic Acids Res 35:7466-74. 2007
    ..Mutations in DNA repair genes and premature aging phenotypes they cause have been reviewed extensively elsewhere, therefore the focus of this review is on the comparison of DNA repair mechanisms in young versus old...
  3. ncbi Making ends meet in old age: DSB repair and aging
    Vera Gorbunova
    Department of Biology, University of Rochester, NY 14627, USA
    Mech Ageing Dev 126:621-8. 2005
    ....
  4. ncbi Distinct tumor suppressor mechanisms evolve in rodent species that differ in size and lifespan
    Andrei Seluanov
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Aging Cell 7:813-23. 2008
    ..Thus, large-bodied species and small but long-lived species have evolved distinct tumor suppressor mechanisms...
  5. ncbi Sirtuin 6 (SIRT6) rescues the decline of homologous recombination repair during replicative senescence
    Zhiyong Mao
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Proc Natl Acad Sci U S A 109:11800-5. 2012
    ..These changes in the processing of DSBs may contribute to age-related genomic instability and a higher incidence of cancer with age. SIRT6 activation provides a potential therapeutic strategy to prevent the decline in genome maintenance...
  6. ncbi Hypersensitivity to contact inhibition provides a clue to cancer resistance of naked mole-rat
    Andrei Seluanov
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Proc Natl Acad Sci U S A 106:19352-7. 2009
    ..We propose that the additional layer of protection conferred by two-tiered contact inhibition contributes to the remarkable tumor resistance of the naked mole-rat...
  7. ncbi Replicatively senescent cells are arrested in G1 and G2 phases
    Zhiyong Mao
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Aging (Albany NY) 4:431-5. 2012
    ..The notion that a large fraction of senescent cell population is arrested in G2 is important for understanding the biology of replicative senescence...
  8. ncbi SIRT6 overexpression induces massive apoptosis in cancer cells but not in normal cells
    Michael Van Meter
    University of Rochester, Rochester, NY, USA
    Cell Cycle 10:3153-8. 2011
    ..These results suggest that SIRT6 is an attractive target for pharmacological activation in cancer treatment...
  9. ncbi Repairing split ends: SIRT6, mono-ADP ribosylation and DNA repair
    Michael Van Meter
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Aging (Albany NY) 3:829-35. 2011
    ..In this research perspective we review the role of SIRT6 in DNA repair and discuss the emerging implications for sirtuin directed mono-ADP ribosylation in aging and age-related diseases...
  10. ncbi Cancer resistance in the blind mole rat is mediated by concerted necrotic cell death mechanism
    Vera Gorbunova
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Proc Natl Acad Sci U S A 109:19392-6. 2012
    ..Thus, we have identified a unique mechanism that contributes to cancer resistance of this subterranean mammal extremely adapted to life underground...
  11. ncbi Rad51 promoter-targeted gene therapy is effective for in vivo visualization and treatment of cancer
    Christopher M Hine
    Department of Biology, University of Rochester, Rochester, New York 14627, USA
    Mol Ther 20:347-55. 2012
    ..This study demonstrates the clinical potential of pRad51-based constructs delivered by nanoparticles for the diagnostics and treatment of a wide range of cancers...
  12. ncbi DNA repair by nonhomologous end joining and homologous recombination during cell cycle in human cells
    Zhiyong Mao
    Department of Biology, University of Rochester, Rochester, New York 14627, USA
    Cell Cycle 7:2902-6. 2008
    ..We conclude that human somatic cells utilize error-prone NHEJ as the major DSB repair pathway at all cell cycle stages, while HR is used, primarily, in the S phase...
  13. ncbi Comparison of nonhomologous end joining and homologous recombination in human cells
    Zhiyong Mao
    Department of Biology, University of Rochester, Rochester, NY 14627 0211, USA
    DNA Repair (Amst) 7:1765-71. 2008
    ..In actively cycling cells NHEJ-C is twice as efficient as NHEJ-I, and NHEJ-I is three times more efficient than HR. Our results suggest that NHEJ is a faster and more efficient DSB repair pathway than HR...
  14. ncbi Coevolution of telomerase activity and body mass in mammals: from mice to beavers
    Vera Gorbunova
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Mech Ageing Dev 130:3-9. 2009
    ..We discuss a model that large body mass presents an increased cancer risk, which drives the evolution of telomerase suppression and replicative senescence...
  15. ncbi TRF2 is required for repair of nontelomeric DNA double-strand breaks by homologous recombination
    Zhiyong Mao
    Department of Biology, University of Rochester, Rochester, NY 14627 0211, USA
    Proc Natl Acad Sci U S A 104:13068-73. 2007
    ..We propose, based on our results and on the ability of TRF2 to mediate strand invasion, that TRF2 plays an essential role in HR by facilitating the formation of early recombination intermediates...
  16. ncbi SIRT6 promotes DNA repair under stress by activating PARP1
    Zhiyong Mao
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Science 332:1443-6. 2011
    ....
  17. ncbi DNA repair by homologous recombination, but not by nonhomologous end joining, is elevated in breast cancer cells
    Zhiyong Mao
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Neoplasia 11:683-91. 2009
    ..Our finding of elevated HR in sporadic breast cancer cell lines suggests that therapies directed against the components of HR will be highly tumor-specific...
  18. ncbi SIRT1 as a therapeutic target in inflammaging of the pulmonary disease
    Irfan Rahman
    Department of Environmental Medicine, Lung Biology and Disease Program, University of Rochester Medical Center, Rochester, NY 14642, USA
    Prev Med 54:S20-8. 2012
    ..The role of dietary polyphenols in regulation of SIRT1 in inflammaging is also discussed...
  19. ncbi Adenoviral vector driven by a minimal Rad51 promoter is selective for p53-deficient tumor cells
    Vincent Fong
    Department of Microbiology and Immunology, University of Rochester, Rochester, New York, United States of America
    PLoS ONE 6:e28714. 2011
    ..The full length Rad51 promoter is highly active in cancer cells but not in normal cells. We therefore set out to assess whether we could confer this tumor-selectivity to an adenovirus vector...
  20. ncbi Changes in the level and distribution of Ku proteins during cellular senescence
    Andrei Seluanov
    Department of Biology, University of Rochester, Rochester, NY 14627 0211, United States
    DNA Repair (Amst) 6:1740-8. 2007
    ....
  21. ncbi Telomerase activity coevolves with body mass not lifespan
    Andrei Seluanov
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Aging Cell 6:45-52. 2007
    ..These results suggest that large body mass presents a greater risk of cancer than long lifespan, and large animals evolve repression of telomerase activity to mitigate that risk...
  22. ncbi Use of the Rad51 promoter for targeted anti-cancer therapy
    Christopher M Hine
    Department of Biology, University of Rochester, Rochester, NY 14627, USA
    Proc Natl Acad Sci U S A 105:20810-5. 2008
    ..Our results suggest that therapies based on the Rad51 promoter will be highly tumor specific and open new avenues for targeting a broad range of cancers...
  23. ncbi Rodents for comparative aging studies: from mice to beavers
    Vera Gorbunova
    Department of Biology, University of Rochester, 213 Hutchison Hall, Rochester, NY, 14627, USA
    Age (Dordr) 30:111-9. 2008
    ..Here we discuss the evolution of lifespan in rodents, review the biology of slow-aging rodents, and show an example of how the use of a comparative approach revealed that telomerase activity coevolved with body mass in rodents...
  24. ncbi Cell divisions are required for L1 retrotransposition
    Xi Shi
    University of Rochester, 213 Hutchison Hall, River Campus, Rochester, NY 14627 0211, USA
    Mol Cell Biol 27:1264-70. 2007
    ..We hypothesize that inhibition of retrotransposition in nondividing cells protects somatic tissues from accumulation of deleterious mutations caused by L1 elements...
  25. ncbi DNA end joining becomes less efficient and more error-prone during cellular senescence
    Andrei Seluanov
    Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA
    Proc Natl Acad Sci U S A 101:7624-9. 2004
    ..We hypothesize that inefficient and aberrant end joining is a likely mechanism underlying the age-related genomic instability and higher incidence of cancer in the elderly...
  26. ncbi Evidence that high telomerase activity may induce a senescent-like growth arrest in human fibroblasts
    Vera Gorbunova
    Huffington Center on Aging, Baylor College of Medicine, Houston, Texas 77030, USA
    J Biol Chem 278:7692-8. 2003
    ..Thus, there must be a critical threshold of telomerase activity that permits cell proliferation...
  27. ncbi Selectable system for monitoring the instability of CTG/CAG triplet repeats in mammalian cells
    Vera Gorbunova
    Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas 77030, USA
    Mol Cell Biol 23:4485-93. 2003
    ..We also discuss how the effect of long CTG/CAG repeat tracts on splicing may contribute to the progression of polyglutamine diseases...
  28. ncbi Telomerase as a growth-promoting factor
    Vera Gorbunova
    Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas, USA
    Cell Cycle 2:534-7. 2003
    ..As some of these functions can be dissociated from telomere lengthening, the question arises as to how the mere presence of telomerase can serve as a survival and growth-promoting factor...
  29. ncbi Genome-wide demethylation promotes triplet repeat instability independently of homologous recombination
    Vincent Dion
    Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA
    DNA Repair (Amst) 7:313-20. 2008
    ..The subtle influences of demethylation on HR at the Aprt locus are not sufficient to account for its dramatic effects on repeat instability. We conclude that 5-aza-CdR promotes triplet repeat instability independently of HR...

Research Grants8

  1. Molecular mechanism of age-related decline of nonhomologous DNA end joining
    Vera Gorbunova; Fiscal Year: 2007
    ..Why genomes become unstable with age is unknown. The proposed study aims to understand the mechanism of age-related genomic instability, which will help develop ways to stabilize the aging genome and prevent cancer. ..
  2. Comparative Analysis of DNA Break Repair in Short- and Long-Lived Rodent Species
    Vera Gorbunova; Fiscal Year: 2010
    ..The information obtained in this study will help to develop strategies to prevent cancer and extend lifespan in humans. ..
  3. Molecular mechanism of age-related decline of nonhomologous DNA end joining
    Vera Gorbunova; Fiscal Year: 2010
    ..Why genomes become unstable with age is unknown. The proposed study aims to understand the mechanism of age-related genomic instability, which will help develop ways to stabilize the aging genome and prevent cancer. ..