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XRCC3 and RAD51 modulate replication fork progression on damaged vertebrate chromosomes.

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XRCC3 and RAD51 modulate replication fork progression on damaged vertebrate chromosomes. / Henry-Mowatt, J.; Jackson, D.; Masson, Y. J.; Johnson, P. A.; Clements, P. M.; Benson, Fiona E.; Thompson, L. H.; Takeda, S.; West, S. C.; Caldecott, K. W.

In: Molecular Cell, Vol. 11, No. 4, 04.2003, p. 1109-1117.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Henry-Mowatt, J, Jackson, D, Masson, YJ, Johnson, PA, Clements, PM, Benson, FE, Thompson, LH, Takeda, S, West, SC & Caldecott, KW 2003, 'XRCC3 and RAD51 modulate replication fork progression on damaged vertebrate chromosomes.', Molecular Cell, vol. 11, no. 4, pp. 1109-1117. https://doi.org/10.1016/S1097-2765(03)00132-1

APA

Henry-Mowatt, J., Jackson, D., Masson, Y. J., Johnson, P. A., Clements, P. M., Benson, F. E., Thompson, L. H., Takeda, S., West, S. C., & Caldecott, K. W. (2003). XRCC3 and RAD51 modulate replication fork progression on damaged vertebrate chromosomes. Molecular Cell, 11(4), 1109-1117. https://doi.org/10.1016/S1097-2765(03)00132-1

Vancouver

Henry-Mowatt J, Jackson D, Masson YJ, Johnson PA, Clements PM, Benson FE et al. XRCC3 and RAD51 modulate replication fork progression on damaged vertebrate chromosomes. Molecular Cell. 2003 Apr;11(4):1109-1117. https://doi.org/10.1016/S1097-2765(03)00132-1

Author

Henry-Mowatt, J. ; Jackson, D. ; Masson, Y. J. ; Johnson, P. A. ; Clements, P. M. ; Benson, Fiona E. ; Thompson, L. H. ; Takeda, S. ; West, S. C. ; Caldecott, K. W. / XRCC3 and RAD51 modulate replication fork progression on damaged vertebrate chromosomes. In: Molecular Cell. 2003 ; Vol. 11, No. 4. pp. 1109-1117.

Bibtex

@article{b813d1c8401f45ceb6646677ce0caf7c,
title = "XRCC3 and RAD51 modulate replication fork progression on damaged vertebrate chromosomes.",
abstract = "The mechanisms by which the progression of eukaryotic replication forks is controlled after DNA damage are unclear. We have found that fork progression is slowed by cisplatin or UV treatment in intact vertebrate cells and in replication assays in vitro. Fork slowing is reduced or absent in irs1SF CHO cells and XRCC3−/− chicken DT40 cells, indicating that fork slowing is an active process that requires the homologous recombination protein XRCC3. The addition of purified human Rad51C-XRCC3 complex restores fork slowing in permeabilized XRCC3−/− cells. Moreover, the requirement for XRCC3 for fork slowing can be circumvented by addition of human Rad51. These data demonstrate that the recombination proteins XRCC3 and Rad51 cooperatively modulate the progression of replication forks on damaged vertebrate chromosomes.",
author = "J. Henry-Mowatt and D. Jackson and Masson, {Y. J.} and Johnson, {P. A.} and Clements, {P. M.} and Benson, {Fiona E.} and Thompson, {L. H.} and S. Takeda and West, {S. C.} and Caldecott, {K. W.}",
year = "2003",
month = apr,
doi = "10.1016/S1097-2765(03)00132-1",
language = "English",
volume = "11",
pages = "1109--1117",
journal = "Molecular Cell",
issn = "1097-2765",
publisher = "Cell Press",
number = "4",

}

RIS

TY - JOUR

T1 - XRCC3 and RAD51 modulate replication fork progression on damaged vertebrate chromosomes.

AU - Henry-Mowatt, J.

AU - Jackson, D.

AU - Masson, Y. J.

AU - Johnson, P. A.

AU - Clements, P. M.

AU - Benson, Fiona E.

AU - Thompson, L. H.

AU - Takeda, S.

AU - West, S. C.

AU - Caldecott, K. W.

PY - 2003/4

Y1 - 2003/4

N2 - The mechanisms by which the progression of eukaryotic replication forks is controlled after DNA damage are unclear. We have found that fork progression is slowed by cisplatin or UV treatment in intact vertebrate cells and in replication assays in vitro. Fork slowing is reduced or absent in irs1SF CHO cells and XRCC3−/− chicken DT40 cells, indicating that fork slowing is an active process that requires the homologous recombination protein XRCC3. The addition of purified human Rad51C-XRCC3 complex restores fork slowing in permeabilized XRCC3−/− cells. Moreover, the requirement for XRCC3 for fork slowing can be circumvented by addition of human Rad51. These data demonstrate that the recombination proteins XRCC3 and Rad51 cooperatively modulate the progression of replication forks on damaged vertebrate chromosomes.

AB - The mechanisms by which the progression of eukaryotic replication forks is controlled after DNA damage are unclear. We have found that fork progression is slowed by cisplatin or UV treatment in intact vertebrate cells and in replication assays in vitro. Fork slowing is reduced or absent in irs1SF CHO cells and XRCC3−/− chicken DT40 cells, indicating that fork slowing is an active process that requires the homologous recombination protein XRCC3. The addition of purified human Rad51C-XRCC3 complex restores fork slowing in permeabilized XRCC3−/− cells. Moreover, the requirement for XRCC3 for fork slowing can be circumvented by addition of human Rad51. These data demonstrate that the recombination proteins XRCC3 and Rad51 cooperatively modulate the progression of replication forks on damaged vertebrate chromosomes.

U2 - 10.1016/S1097-2765(03)00132-1

DO - 10.1016/S1097-2765(03)00132-1

M3 - Journal article

VL - 11

SP - 1109

EP - 1117

JO - Molecular Cell

JF - Molecular Cell

SN - 1097-2765

IS - 4

ER -