Titlebook: DNA Damage and Repair; Advances from Phage Jac A. Nickoloff,Merl F. Hoekstra Book 2001 Springer Science+Business Media New York 2001 DNA.D

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Kisha Supernant,Jane Eva Baxter,Sonya Atalayortant not only in maintaining the integrity of nuclear DNA but also in protecting mitochondrial DNA against oxidative onslaught from FADH. and NADH and the reactive oxygen species generated during O. reduction .. Estimates of the number of abasic sites generated per mammalian cell per day run as hi

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Sherene Baugher,Suzanne M. Spencer-Woodhaploid cells, and ...α in diploid cells. .α and . a each have two open reading frames, but functions have only been identified for three gene products, Mat.1p, Matα1p, and Matα2p. The . gene products are key regulators of the different stages of the yeast life cycle (reviewed in refs. .,.,.). The M

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https://doi.org/10.1007/978-1-4419-1501-6been dramatic. This is attributable in part to the analysis of DSB repair-deficient rodent cell lines, which led to the isolation and characterization of the DNA-PK complex, XRCC4, DNA ligase IV, and others .. The gene products thus identified have provided many important insights regarding the func

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Gary M. Feinman,T. Douglas Pricebreaks (DSBs) in yeast are potent inducers of homologous recombination and that homologous recombination is the major pathway in yeast to repair DSBs (Chapter 16, Vol. 1). Compared with nonhomologous repair, homologous recombination has generally been considered to be inconsequential as a DSB repair

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Gary M. Feinman,T. Douglas Pricehis task, lymphocytes express clonally unique antigen receptors that transduce signals that activate humoral (B cell) or cellular (T cell) effector functions upon recognition of a suitable antigenic ligand. Lymphocytes require the faithful execution of DNA repair processes first to generate, and the

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The Transition to Food Productionutagens can cause a variety of DNA lesions, including base modifications, intra- and interstrand crosslinks and single- or double-strand breaks .. If left unrepaired, these DNA lesions can lead to mutations or loss of viability. Thus, cell-cycle checkpoints and DNA-repair mechanisms have evolved to