Establishment of a monoclonal antibody recognizing cyclobutane-type thymine dimers in DNA: a comparative study with 64M-1 antibody specific for (6-4) photoproducts

Mizuno, Takuya; Matsunaga, Tsukasa; Ihara, Masataka; Nikaido, Osamu

doi:10.1016/0921-8777(91)90009-e

Cited by 88 publications

(50 citation statements)

References 34 publications

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“…Quantitative analyses of the excision data in lanes 6 and 8 of Fig. 1B and of several experiments conducted under identical conditions reveal that the T T photolesion is repaired threefold faster than the TϽϾT photoproduct, in agreement with the relative rates of removal of these lesions in vivo (42,43). The excision rate and pattern of cisplatin 1,2-d(GpG) cross-link are comparable to those of T T and have been reported previously (27,68).…”

Section: Resultssupporting

confidence: 66%

Recognition and Repair of Compound DNA Lesions (Base Damage and Mismatch) by Human Mismatch Repair and Excision Repair Systems

Tursun

Duckett

et al. 1997

Molecular and Cellular Biology

184

133

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Nucleotide excision repair and the long-patch mismatch repair systems correct abnormal DNA structures arising from DNA damage and replication errors, respectively. DNA synthesis past a damaged base (translesion replication) often causes misincorporation at the lesion site. In addition, mismatches are hot spots for DNA damage because of increased susceptibility of unpaired bases to chemical modification. We call such a DNA lesion, that is, a base damage superimposed on a mismatch, a compound lesion. To learn about the processing of compound lesions by human cells, synthetic compound lesions containing UV photoproducts or cisplatin 1,2-d(GpG) intrastrand cross-link and mismatch were tested for binding to the human mismatch recognition complex hMutS␣ and for excision by the human excision nuclease. No functional overlap between excision repair and mismatch repair was observed. The presence of a thymine dimer or a cisplatin diadduct in the context of a G-T mismatch reduced the affinity of hMutS␣ for the mismatch. In contrast, the damaged bases in these compound lesions were excised three-to fourfold faster than simple lesions by the human excision nuclease, regardless of the presence of hMutS␣ in the reaction. These results provide a new perspective on how excision repair, a cellular defense system for maintaining genomic integrity, can fix mutations under certain circumstances.Mismatches in DNA resulting from replication errors, and base damage caused by physical (UV light) and chemical (polyaromatic hydrocarbons) agents, are responsible for the majority of human cancers (18). Although certain mismatches and base lesions can be eliminated from DNA by the base excision repair pathway initiated by glycosylases with narrow substrate ranges, in human cells there exists a general mismatch repair system and a general damage repair system of wide substrate range. The mismatch repair system removes the mismatched base as a nucleotide (44), and the excision repair system excises the damaged base(s) in an oligonucleotide (52, 67).The general mismatch repair system (long-patch mismatch repair) corrects all eight single-base mismatches as well as small insertion sequence loops with comparable efficiencies (31, 44). The general nucleotide excision repair (excision repair) system (8) not only is the sole repair pathway for bulky lesions such as thymine dimers (TϽϾT) and cisplatin-guanine adducts but also repairs a wide variety of nonbulky lesions such as O 6 -methylguanine (O 6 -meG) at physiologically relevant rates (52). Thus, it appears that both repair systems recognize many dissimilar non-B DNA forms rather than a specific lesion structure.Given the wide substrate ranges of both systems, it is not unreasonable to expect overlaps between the two substrate spectra, or that one repair system may facilitate the function of the other. Indeed, it has been shown that the excision repair system recognizes mismatches and removes the mismatched base in a manner identical to the removal of damaged bases (27). Since a DNA lesion, by de...

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Section: Resultssupporting

confidence: 66%

Recognition and Repair of Compound DNA Lesions (Base Damage and Mismatch) by Human Mismatch Repair and Excision Repair Systems

Tursun

Duckett

et al. 1997

Molecular and Cellular Biology

184

133

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“…Nine distinct mouse monoclonal antibodies have been generated in our laboratory, each specific for CPDs, 6-4PPs or Dewar isomers (Table 1) (34)(35)(36)(37)(38). We established TDM-2, TDM-3, 64M-2, 64M-3, 64M-4, and 64M-5 antibodies from BALB/c mice (37).…”

Section: Monoclonal Antibodiesmentioning

confidence: 99%

“…An immunological assay is an indirect method in which selective binding of an antibody to the corresponding antigen is essential and monoclonal antibodies are the most specific probes. We thus raised monoclonal antibodies against each type of DNA damage, CPDs, 6-4PPs or Dewar isomers (34)(35)(36)(37)(38). We have also established an enzyme-linked immunosorbent assay (ELISA) for reliable and sensitive quantitation of these photoproducts (37,38).…”

Section: Introductionmentioning

confidence: 99%

Quantitation and Visualization of Ultraviolet‐Induced DNA Damage Using Specific Antibodies: Application to Pigment Cell Biology

Kobayashi

Katsumi

Imoto

et al. 2001

Pigment Cell Research

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The major types of DNA damage induced by sunlight in the scope. This latter method allows us to reconstruct three-diskin are DNA photoproducts, such as cyclobutane pyrimidine mensional images of nuclei containing DNA photoproducts and to simultaneously examine DNA photoproducts and hisdimers (CPDs), (6-4)photoproducts (6-4PPs) and Dewar isotology in multilayered epidermis. Using those techniques, one mers of 6-4PPs. A sensitive method for quantitating and can determine the induction and repair of these three distinct visualizing each type of DNA photoproduct induced by biologtypes of DNA photoproducts in cultured cells and in the skin ically relevant doses of ultraviolet (UV) or sunlight is essential to characterize DNA photoproducts and their biological efexposed to sublethal or suberythematous doses of UV or solar simulated radiation. As examples of the utility of these techfects. We have established monoclonal antibodies specific for niques and antibodies, we describe the DNA repair kinetics CPDs, 6-4PPs or Dewar isomers. Those antibodies allow one to quantitate photoproducts in DNA purified from cultured following irradiation of human cell nuclei and the photoprotective effect of melanin against DNA photoproducts in cultured cells or from the skin epidermis using an enzyme-linked immunosorbent assay. One can also use those specific antibodpigmented cells and in human epidermis. ies with in situ laser cytometry to visualize and measure DNA

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“…To estimate the DNA repair capacity of the cells, the levels of CPD and 6-4PP were measured in UVC-and UVB-irradiated cells by the enzyme-linked immunosorbent assay (ELISA), as previously described. 10,17,19,20) Briefly, to measure the level of CPD, DNA was extracted from the cells at the indicated times after UVC (10 J/m 2 ) and UVB (38 J/m 2 ) irradiation using a DNeasy Tissue kit (QIAGEN, Hilden, Germany). The DNA concentration was quantified by measuring the absorbance at 260 nm.…”

Section: Methodsmentioning

confidence: 99%

The Involvement of Annexin II in Resistance to UVB-Induced Cell Death and in the Increased Nucleotide Excision Repair Capacity of UV-Damaged DNA in Human Cells

Yano

Chen

Kita

et al. 2013

Bioscience, Biotechnology, and Biochemistry

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Establishment of a monoclonal antibody recognizing cyclobutane-type thymine dimers in DNA: a comparative study with 64M-1 antibody specific for (6-4) photoproducts

Cited by 88 publications

References 34 publications

Recognition and Repair of Compound DNA Lesions (Base Damage and Mismatch) by Human Mismatch Repair and Excision Repair Systems

Recognition and Repair of Compound DNA Lesions (Base Damage and Mismatch) by Human Mismatch Repair and Excision Repair Systems

Quantitation and Visualization of Ultraviolet‐Induced DNA Damage Using Specific Antibodies: Application to Pigment Cell Biology

The Involvement of Annexin II in Resistance to UVB-Induced Cell Death and in the Increased Nucleotide Excision Repair Capacity of UV-Damaged DNA in Human Cells

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