Cell divisions are required for L1 retrotranspositionXi 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...
CLK-1 protein has DNA binding activity specific to O(L) region of mitochondrial DNAVera Gorbunova
Huffington Center on Aging, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA
FEBS Lett 516:279-84. 2002
..Our results suggest that, in addition to its enzymatic function in ubiquinone biosynthesis, CLK-1 is involved in the regulation of mtDNA replication or transcription...
- 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...
- 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...
- 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...
- 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...
- 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...
- Genome-wide demethylation destabilizes CTG.CAG trinucleotide repeats in mammalian cells
Vera Gorbunova
Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA
Hum Mol Genet 13:2979-89. 2004
..The dramatic destabilizing effect of DNA methyltransferase inhibitors supports the hypothesis that changes in methylation patterns during epigenetic reprogramming may trigger the intergenerational repeat expansions that lead to disease...
- 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...
- 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...
- 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
....
- 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
....
- 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...
