Repair of Thymine Dimers and (6–4) Photoproducts in Group a Xeroderma Pigmentosum Cell Lines Harboring a Transferred Normal Chromosome 9

Ishizaki, Kanji; Matsunaga, Tsukasa; Kato, Mitsuo; Nikaido, Osamu; Ikenaga, Mituo

doi:10.1111/j.1751-1097.1992.tb02172.x

Cited by 9 publications

(1 citation statement)

References 22 publications

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“…The greatest contribution of dimer antibodies has been in the field of “UV effects,” a catch‐all term for a plethora of biological responses to UVR. Immunoassays have been applied to various facets of the DNA damage response in many different living systems, including phage (105–108), archaea (109–111), bacteria (53,112–123), protists (124–126), yeast and mold (127–133), algae and higher plants (134–155), nematodes (156,157), echinoderms (158,159), crustaceans (160–162), insects (163), frogs (164), fish (81,165–173), marsupials (174), rodents (4,6,175–210) and humans (4,6,14,211–247). Antibodies specific to CPDs and (6‐4) PDs have contributed, more than any other reagents, to our understanding of the biological response to DNA damage, including DNA repair and the pathological consequences of its partial or complete abrogation.…”

Section: Uv Effectsmentioning

confidence: 99%

Antibodies and DNA Photoproducts: Applications, Milestones and Reference Guide

Mitchell¹,

Brooks

2010

Photochem & Photobiology

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Polyclonal and monoclonal antibodies recognizing the primary DNA photoproducts induced by ultraviolet radiation (UVR) have proven to be essential tools in the study of photochemical and photobiological phenomena. As specific ''DNA damage binding proteins'' these reagents have been used to develop a diverse array of technical procedures applied to a plethora of important problems in DNA photochemistry and the biological effects of UVR at the molecular, developmental, organism and population levels. This survey attempts to cover this science from an historical perspective and to reveal the great breadth of discovery and contribution associated with the development and application of DNA damage antibodies to the current body of science.Three papers published in the 1960s were seminal to the development of immunoassays for the study of photochemical and photobiological phenomena. In 1960 Rosalyn Yalow and Solomon Berson published a paper in the Journal of Clinical Investigation entitled ''Immunoassay of endogenous plasma insulin in man'' (1), which described the development of a sensitive radioimmunoassay (RIA) to measure minute quantities of hormones in blood samples. This technique played a seminal role in the exponential expansion of research in medicine and the biological sciences over the past half century. In 1977 Dr. Yalow was awarded the Nobel Prize in Medicine for her work. In 1964 Otto Plescia and colleagues published a paper in the Proceedings of the National Academy of Sciences entitled ''Production of antibodies to denatured deoxyribonucleic acid (DNA)'' (2). Using a technique whereby singlestranded DNA was electrostatically coupled to methylated bovine serum albumin they were able to elicit an immune response in rabbits. In the wake of this paper it was not long before a group led by Lawrence Levine and Helen van Vanukis published an article in Science in 1966 entitled ''Antibodies to photoproducts of deoxyribonucleic acids irradiated with ultraviolet light'' (3). Using the technique established by Plescia, this group was able to produce a rabbit antiserum using DNA irradiated with 270 nm light with antigenic determinants that were reversible by 235 nm light and responsive to UV-irradiated thymidine nucleotides. It appeared that antibodies had been created in response to thymine dimers.Over the course of the following two decades a number of polyclonal and monoclonal antibodies to various UV-induced DNA lesions were produced and characterized. The technology that developed blossomed and has been applied to a broad spectrum of problems in photochemistry, the biological response to UV radiation (UVR), photomedicine and environmental photobiology. Early immunoassays generated DNA repair curves showing rapid removal of most antibody binding sites leaving behind a significant remnant (4,5). These results were not consistent with the known repair kinetics using biochemical and enzymatic techniques. Subsequently, it was discovered that polyclonal antisera raised against heavily UVirradiated DNA contai...

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Section: Uv Effectsmentioning

confidence: 99%

Antibodies and DNA Photoproducts: Applications, Milestones and Reference Guide

Mitchell¹,

Brooks

2010

Photochem & Photobiology

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Increased UV‐induced SCEs but normal repair of DNA damage in p53‐deficient mouse cells

Ishizaki

Ejima

Matsunaga

et al. 1994

Intl Journal of Cancer

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UV-induced sister chromatid exchanges (SCEs) in p53-deficient mouse cells were studied to obtain more evidence regarding the involvement of p53 protein in the DNA repair pathway as a checkpoint protein. After 5 J/m2 UV irradiation, mutant-type homozygous cells for p53-deficiency showed the same number of SCEs as the heterozygous and wild-type homozygous cells. In the heterozygous and wild-type homozygous cells, no further increase of SCEs was observed after 10 J/m2 UV irradiation. In contrast, in mutant-type homozygous cells about twice as many SCEs were induced by 10 J/m2 UV as by 5 J/m2 UV. In mutant-type homozygous cells, fractions of S-phase cells decreased just after 10 J/m2 UV irradiation, but recovered to higher than control levels within a short time, while in heterozygous and wild-type homozygous cells, the decrease in S-phase cells was prolonged by more than 6 hr and no increase above control levels was observed. Although no difference in UV sensitivity and repair of UV-induced DNA damage was found among the 3 genotypes, which were determined by the relative colony-forming ability after UV irradiation and removal of thymine dimers and (6-4) photoproducts from cellular DNA, our data strongly suggest an impaired checkpoint function in p53-deficient cells when DNA is damaged.

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