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Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress

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Standard

Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress. / Kristensen, Hans-Ulrik Svejstrup; Epanchintsev, Alexey; Rauschendorf, Marc-Alexander; Laugel, Vincent; Stevnsner, Tinna; Bohr, Vilhelm A; Coin, Frederic; Egly, Jean-Marc.

I: Proceedings of the National Academy of Sciences of the United States of America, Bind 110, Nr. 25, 18.06.2013, s. 2261-2270.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Harvard

Kristensen, H-US, Epanchintsev, A, Rauschendorf, M-A, Laugel, V, Stevnsner, T, Bohr, VA, Coin, F & Egly, J-M 2013, 'Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress', Proceedings of the National Academy of Sciences of the United States of America, bind 110, nr. 25, s. 2261-2270. https://doi.org/10.1073/pnas.1220071110

APA

Kristensen, H-U. S., Epanchintsev, A., Rauschendorf, M-A., Laugel, V., Stevnsner, T., Bohr, V. A., ... Egly, J-M. (2013). Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress. Proceedings of the National Academy of Sciences of the United States of America, 110(25), 2261-2270. https://doi.org/10.1073/pnas.1220071110

CBE

Kristensen H-US, Epanchintsev A, Rauschendorf M-A, Laugel V, Stevnsner T, Bohr VA, Coin F, Egly J-M. 2013. Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress. Proceedings of the National Academy of Sciences of the United States of America. 110(25):2261-2270. https://doi.org/10.1073/pnas.1220071110

MLA

Kristensen, Hans-Ulrik Svejstrup o.a.. "Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress". Proceedings of the National Academy of Sciences of the United States of America. 2013, 110(25). 2261-2270. https://doi.org/10.1073/pnas.1220071110

Vancouver

Kristensen H-US, Epanchintsev A, Rauschendorf M-A, Laugel V, Stevnsner T, Bohr VA o.a. Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress. Proceedings of the National Academy of Sciences of the United States of America. 2013 jun 18;110(25):2261-2270. https://doi.org/10.1073/pnas.1220071110

Author

Kristensen, Hans-Ulrik Svejstrup ; Epanchintsev, Alexey ; Rauschendorf, Marc-Alexander ; Laugel, Vincent ; Stevnsner, Tinna ; Bohr, Vilhelm A ; Coin, Frederic ; Egly, Jean-Marc. / Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress. I: Proceedings of the National Academy of Sciences of the United States of America. 2013 ; Bind 110, Nr. 25. s. 2261-2270.

Bibtex

@article{3ec3012c0f7a482eba279016cc09d259,
title = "Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress",
abstract = "Cockayne syndrome type B ATPase (CSB) belongs to the SwItch/Sucrose nonfermentable family. Its mutations are linked to Cockayne syndrome phenotypes and classically are thought to be caused by defects in transcription-coupled repair, a subtype of DNA repair. Here we show that after UV-C irradiation, immediate early genes such as activating transcription factor 3 (ATF3) are overexpressed. Although the ATF3 target genes, including dihydrofolate reductase (DHFR), were unable to recover RNA synthesis in CSB-deficient cells, transcription was restored rapidly in normal cells. There the synthesis of DHFR mRNA restarts on the arrival of RNA polymerase II and CSB and the subsequent release of ATF3 from its cAMP response element/ATF target site. In CSB-deficient cells ATF3 remains bound to the promoter, thereby preventing the arrival of polymerase II and the restart of transcription. Silencing of ATF3, as well as stable introduction of wild-type CSB, restores RNA synthesis in UV-irradiated CSB cells, suggesting that, in addition to its role in DNA repair, CSB activity likely is involved in the reversal of inhibitory properties on a gene-promoter region. We present strong experimental data supporting our view that the transcriptional defects observed in UV-irradiated CSB cells are largely the result of a permanent transcriptional repression of a certain set of genes in addition to some defect in DNA repair.",
author = "Kristensen, {Hans-Ulrik Svejstrup} and Alexey Epanchintsev and Marc-Alexander Rauschendorf and Vincent Laugel and Tinna Stevnsner and Bohr, {Vilhelm A} and Frederic Coin and Jean-Marc Egly",
year = "2013",
month = "6",
day = "18",
doi = "10.1073/pnas.1220071110",
language = "English",
volume = "110",
pages = "2261--2270",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
publisher = "The National Academy of Sciences of the United States of America",
number = "25",

}

RIS

TY - JOUR

T1 - Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress

AU - Kristensen, Hans-Ulrik Svejstrup

AU - Epanchintsev, Alexey

AU - Rauschendorf, Marc-Alexander

AU - Laugel, Vincent

AU - Stevnsner, Tinna

AU - Bohr, Vilhelm A

AU - Coin, Frederic

AU - Egly, Jean-Marc

PY - 2013/6/18

Y1 - 2013/6/18

N2 - Cockayne syndrome type B ATPase (CSB) belongs to the SwItch/Sucrose nonfermentable family. Its mutations are linked to Cockayne syndrome phenotypes and classically are thought to be caused by defects in transcription-coupled repair, a subtype of DNA repair. Here we show that after UV-C irradiation, immediate early genes such as activating transcription factor 3 (ATF3) are overexpressed. Although the ATF3 target genes, including dihydrofolate reductase (DHFR), were unable to recover RNA synthesis in CSB-deficient cells, transcription was restored rapidly in normal cells. There the synthesis of DHFR mRNA restarts on the arrival of RNA polymerase II and CSB and the subsequent release of ATF3 from its cAMP response element/ATF target site. In CSB-deficient cells ATF3 remains bound to the promoter, thereby preventing the arrival of polymerase II and the restart of transcription. Silencing of ATF3, as well as stable introduction of wild-type CSB, restores RNA synthesis in UV-irradiated CSB cells, suggesting that, in addition to its role in DNA repair, CSB activity likely is involved in the reversal of inhibitory properties on a gene-promoter region. We present strong experimental data supporting our view that the transcriptional defects observed in UV-irradiated CSB cells are largely the result of a permanent transcriptional repression of a certain set of genes in addition to some defect in DNA repair.

AB - Cockayne syndrome type B ATPase (CSB) belongs to the SwItch/Sucrose nonfermentable family. Its mutations are linked to Cockayne syndrome phenotypes and classically are thought to be caused by defects in transcription-coupled repair, a subtype of DNA repair. Here we show that after UV-C irradiation, immediate early genes such as activating transcription factor 3 (ATF3) are overexpressed. Although the ATF3 target genes, including dihydrofolate reductase (DHFR), were unable to recover RNA synthesis in CSB-deficient cells, transcription was restored rapidly in normal cells. There the synthesis of DHFR mRNA restarts on the arrival of RNA polymerase II and CSB and the subsequent release of ATF3 from its cAMP response element/ATF target site. In CSB-deficient cells ATF3 remains bound to the promoter, thereby preventing the arrival of polymerase II and the restart of transcription. Silencing of ATF3, as well as stable introduction of wild-type CSB, restores RNA synthesis in UV-irradiated CSB cells, suggesting that, in addition to its role in DNA repair, CSB activity likely is involved in the reversal of inhibitory properties on a gene-promoter region. We present strong experimental data supporting our view that the transcriptional defects observed in UV-irradiated CSB cells are largely the result of a permanent transcriptional repression of a certain set of genes in addition to some defect in DNA repair.

U2 - 10.1073/pnas.1220071110

DO - 10.1073/pnas.1220071110

M3 - Journal article

C2 - 23733932

VL - 110

SP - 2261

EP - 2270

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 25

ER -