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Role for non-homologous end-joining in the repair of UVA induced damage.

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Role for non-homologous end-joining in the repair of UVA induced damage. / Fell, L. J.; Paul, N. D.; McMillan, T. J.
In: International Journal of Radiation Biology, Vol. 78, No. 11, 11.2002, p. 1023-1027.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Harvard

Fell, LJ, Paul, ND & McMillan, TJ 2002, 'Role for non-homologous end-joining in the repair of UVA induced damage.', International Journal of Radiation Biology, vol. 78, no. 11, pp. 1023-1027. https://doi.org/10.1080/0955300021000016558

APA

Fell, L. J., Paul, N. D., & McMillan, T. J. (2002). Role for non-homologous end-joining in the repair of UVA induced damage. International Journal of Radiation Biology, 78(11), 1023-1027. https://doi.org/10.1080/0955300021000016558

Vancouver

Fell LJ, Paul ND, McMillan TJ. Role for non-homologous end-joining in the repair of UVA induced damage. International Journal of Radiation Biology. 2002 Nov;78(11):1023-1027. doi: 10.1080/0955300021000016558

Author

Fell, L. J. ; Paul, N. D. ; McMillan, T. J. / Role for non-homologous end-joining in the repair of UVA induced damage. In: International Journal of Radiation Biology. 2002 ; Vol. 78, No. 11. pp. 1023-1027.

Bibtex

@article{6485a42c9ef74c8fa0bf2ebbb3b6bc40,
title = "Role for non-homologous end-joining in the repair of UVA induced damage.",
abstract = "Purpose : The biological significance of long-wavelength ultraviolet (UV) light, UVA, is increasingly realized, but the precise nature of the cellular damage responsible for the effects of this radiation is still not clear. It has been reported that UVA can induce double-strand breaks in DNA, but the biological significance of these is not known. We have therefore examined the UVA sensitivity of a cell line deficient in non-homologous end-joining, the major pathway for the repair of DNA double-strand breaks in mammalian cells in order to determine the biological importance of UVA-induced DSB. Materials and methods : Xrs-6, a Chinese hamster ovary cell line mutant for XRCC5 (Ku80) was compared with its parental CHO-K1 cell line for its sensitivity to UVA radiation (365 nm) using both a clonogenic assay and the micronucleus assay. Results : Xrs-6 cells were sensitive to the cytotoxic effects of UVA. This resulted in the formation of chromosome damage, as measured by the micronucleus assay, which this cell line was unable to repair. Conclusions : Owing to the nature of the repair defect in these cells, these results imply that DNA double-strand breaks are produced in cells following UVA irradiation, that the non-homologous end-joining repair pathway is involved in their repair and that they are produced with sufficient frequency to have biological significance.",
author = "Fell, {L. J.} and Paul, {N. D.} and McMillan, {T. J.}",
year = "2002",
month = nov,
doi = "10.1080/0955300021000016558",
language = "English",
volume = "78",
pages = "1023--1027",
journal = "International Journal of Radiation Biology",
issn = "0955-3002",
publisher = "Informa Healthcare",
number = "11",

}

RIS

TY - JOUR

T1 - Role for non-homologous end-joining in the repair of UVA induced damage.

AU - Fell, L. J.

AU - Paul, N. D.

AU - McMillan, T. J.

PY - 2002/11

Y1 - 2002/11

N2 - Purpose : The biological significance of long-wavelength ultraviolet (UV) light, UVA, is increasingly realized, but the precise nature of the cellular damage responsible for the effects of this radiation is still not clear. It has been reported that UVA can induce double-strand breaks in DNA, but the biological significance of these is not known. We have therefore examined the UVA sensitivity of a cell line deficient in non-homologous end-joining, the major pathway for the repair of DNA double-strand breaks in mammalian cells in order to determine the biological importance of UVA-induced DSB. Materials and methods : Xrs-6, a Chinese hamster ovary cell line mutant for XRCC5 (Ku80) was compared with its parental CHO-K1 cell line for its sensitivity to UVA radiation (365 nm) using both a clonogenic assay and the micronucleus assay. Results : Xrs-6 cells were sensitive to the cytotoxic effects of UVA. This resulted in the formation of chromosome damage, as measured by the micronucleus assay, which this cell line was unable to repair. Conclusions : Owing to the nature of the repair defect in these cells, these results imply that DNA double-strand breaks are produced in cells following UVA irradiation, that the non-homologous end-joining repair pathway is involved in their repair and that they are produced with sufficient frequency to have biological significance.

AB - Purpose : The biological significance of long-wavelength ultraviolet (UV) light, UVA, is increasingly realized, but the precise nature of the cellular damage responsible for the effects of this radiation is still not clear. It has been reported that UVA can induce double-strand breaks in DNA, but the biological significance of these is not known. We have therefore examined the UVA sensitivity of a cell line deficient in non-homologous end-joining, the major pathway for the repair of DNA double-strand breaks in mammalian cells in order to determine the biological importance of UVA-induced DSB. Materials and methods : Xrs-6, a Chinese hamster ovary cell line mutant for XRCC5 (Ku80) was compared with its parental CHO-K1 cell line for its sensitivity to UVA radiation (365 nm) using both a clonogenic assay and the micronucleus assay. Results : Xrs-6 cells were sensitive to the cytotoxic effects of UVA. This resulted in the formation of chromosome damage, as measured by the micronucleus assay, which this cell line was unable to repair. Conclusions : Owing to the nature of the repair defect in these cells, these results imply that DNA double-strand breaks are produced in cells following UVA irradiation, that the non-homologous end-joining repair pathway is involved in their repair and that they are produced with sufficient frequency to have biological significance.

U2 - 10.1080/0955300021000016558

DO - 10.1080/0955300021000016558

M3 - Journal article

VL - 78

SP - 1023

EP - 1027

JO - International Journal of Radiation Biology

JF - International Journal of Radiation Biology

SN - 0955-3002

IS - 11

ER -