A xeroderma pigmentosum complementation group A related gene: confirmation using monoclonal antibodies against the cyclobutane dimer and (6-4) photoproduct

Mori, Toshio; Rinaldy, T.L.; Athwal, Raghbir S.; Kaur, Gagandeep; Nikaido, Osamu; Lloyd, R. Stephen; Rinaldy, Augustinus

doi:10.1016/0921-8777(93)90065-o

Cited by 11 publications

(2 citation statements)

References 40 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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“…Under their experimental conditions, both VA13 and GM637 cells rapidly remove 6-4PPs, as expected. However, they also both remove more than 50% of the CPDs from genomic DNA 24 h after exposure of cells to 10 J/m 2 UV light [42,43]. In addition, Evano et al [44] measured UV photoproduct removal in wild-type MRC5 and C5RO primary human ®broblasts and their respective SV40-transformed derivatives as part of a study on the removal of UV photoproducts in XP and trichothiodystrophy cells.…”

Section: DI Is Sc Cu Us Ss Si Io On Nmentioning

confidence: 99%

Reduced global genomic repair of ultraviolet light-induced cyclobutane pyrimidine dimers in simian virus 40-transformed human cells

et al. 2000

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The p53 tumor‐suppressor gene has been implicated in the inducible activation of excision repair of ultraviolet (UV)‐induced cyclobutane pyrimidine dimers (CPDs) in human cells. Because the large T antigen (LTAg) of the simian virus 40 (SV40) binds p53 protein and can interfere with its function, it was of interest to study DNA repair in normal human fibroblasts that had been transformed by SV40 compared with that in their nontransformed parental counterparts and to determine whether such transformation attenuated global genomic repair (GGR) of CPDs. Three methods were used to measure GGR in UV‐irradiated cells: (i) an immunoassay using monoclonal antibodies specific for CPDs or 6‐4 photoproducts (6‐4PPs), (ii) zone sedimentation in alkaline sucrose gradients to measure the average DNA strand size after specific nicking at CPD sites in duplex DNA with T4 endonuclease V (TEV), and (iii) Southern hybridization of TEV‐treated DNA with strand‐specific mRNA probes to assess removal of CPDs from either strand of a defined genetic sequence in an expressed gene. Whereas repair of 6‐4PPs was very similar in paired SV40‐transformed and primary fibroblasts, GGR of CPDs was significantly reduced in the SV40‐transformed cells. In contrast, SV40 transformation did not appreciably affect the efficiency of transcription‐coupled repair. These data support the hypothesis that SV40 transformation can result in reduced levels of GGR, most likely because of the inhibition of normal p53 function by LTAg. Mol. Carcinog. 29:17–24, 2000. © 2000 Wiley‐Liss, Inc.

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Mutation and expression of theXPA gene in revertants and hybrids of a xeroderma pigmentosum cell line

Cleaver

McDowell

Jones

et al. 1994

Somat Cell Mol Genet

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A series of ultraviolet (UV)-resistant cell lines have been generated from a UV-sensitive XP group A cell line homozygous for a stop codon (TGA) in the chromosome 9 XPA gene. Three lines generated by chemical mutagenesis acquired the ability to excise (6-4) photoproducts but not cyclobutane dimers from the whole genome; two lines generated by a fusion procedure with hamster cells acquired the ability to excise both (6-4) photoproducts and cyclobutane dimers from the whole genome. A central region of the hamster XPA gene was cloned and sequenced. With the use of species-specific primers in the polymerase chain reaction, we found that the hybrid cell lines do not contain a hamster XPA gene. Sequence analysis showed that all of the UV-resistant cell lines contain reversions of the human stop codon, resulting in missense mutations (glycine or leucine for arginine) or wild-type sequences. The concentration of XPA protein in revertant cell lines was about one-half that in normal cells, which would be expected from heterozygous cells; there was no evidence that the mutant proteins were less stable than the wild-type proteins. These results are consistent with the idea that the XPA protein initiates repair by binding to damaged sites with various affinities, depending on the photoproduct and the transcriptional state of the region. A concentration of XPA protein near 50% is needed before repair can proceed into nontranscribed regions of the genome. The revertant cell lines represent a class of missense mutations in the XPA gene that may have altered specificity and that can be used to understand some of the regulatory differences in repair of photoproducts in various regions of the genome.

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A xeroderma pigmentosum complementation group A related gene: confirmation using monoclonal antibodies against the cyclobutane dimer and (6-4) photoproduct

Cited by 11 publications

References 40 publications

Antibodies and DNA Photoproducts: Applications, Milestones and Reference Guide

Antibodies and DNA Photoproducts: Applications, Milestones and Reference Guide

Reduced global genomic repair of ultraviolet light-induced cyclobutane pyrimidine dimers in simian virus 40-transformed human cells

Mutation and expression of theXPA gene in revertants and hybrids of a xeroderma pigmentosum cell line

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