Overexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner

Oncogene-induced replication stress (RS) promotes cancer development. Here, the authors report that cancer cells adapt to oncogene-induced RS by overexpressing downstream components of ATR-CHK1 pathway, Claspin and Timeless, which have protective role at the replication forks independent of their ch...

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Autores principales: Julien N. Bianco, Valérie Bergoglio, Yea-Lih Lin, Marie-Jeanne Pillaire, Anne-Lyne Schmitz, Julia Gilhodes, Amelie Lusque, Julien Mazières, Magali Lacroix-Triki, Theodoros I. Roumeliotis, Jyoti Choudhary, Jérôme Moreaux, Jean-Sébastien Hoffmann, Hélène Tourrière, Philippe Pasero
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Publicado: Nature Portfolio 2019
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Acceso en línea:https://doaj.org/article/fdf314771754477295f673e54990011e
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spelling oai:doaj.org-article:fdf314771754477295f673e54990011e2021-12-02T15:35:53ZOverexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner10.1038/s41467-019-08886-82041-1723https://doaj.org/article/fdf314771754477295f673e54990011e2019-02-01T00:00:00Zhttps://doi.org/10.1038/s41467-019-08886-8https://doaj.org/toc/2041-1723Oncogene-induced replication stress (RS) promotes cancer development. Here, the authors report that cancer cells adapt to oncogene-induced RS by overexpressing downstream components of ATR-CHK1 pathway, Claspin and Timeless, which have protective role at the replication forks independent of their checkpoint function.Julien N. BiancoValérie BergoglioYea-Lih LinMarie-Jeanne PillaireAnne-Lyne SchmitzJulia GilhodesAmelie LusqueJulien MazièresMagali Lacroix-TrikiTheodoros I. RoumeliotisJyoti ChoudharyJérôme MoreauxJean-Sébastien HoffmannHélène TourrièrePhilippe PaseroNature PortfolioarticleScienceQENNature Communications, Vol 10, Iss 1, Pp 1-14 (2019)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Julien N. Bianco
Valérie Bergoglio
Yea-Lih Lin
Marie-Jeanne Pillaire
Anne-Lyne Schmitz
Julia Gilhodes
Amelie Lusque
Julien Mazières
Magali Lacroix-Triki
Theodoros I. Roumeliotis
Jyoti Choudhary
Jérôme Moreaux
Jean-Sébastien Hoffmann
Hélène Tourrière
Philippe Pasero
Overexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner
description Oncogene-induced replication stress (RS) promotes cancer development. Here, the authors report that cancer cells adapt to oncogene-induced RS by overexpressing downstream components of ATR-CHK1 pathway, Claspin and Timeless, which have protective role at the replication forks independent of their checkpoint function.
format article
author Julien N. Bianco
Valérie Bergoglio
Yea-Lih Lin
Marie-Jeanne Pillaire
Anne-Lyne Schmitz
Julia Gilhodes
Amelie Lusque
Julien Mazières
Magali Lacroix-Triki
Theodoros I. Roumeliotis
Jyoti Choudhary
Jérôme Moreaux
Jean-Sébastien Hoffmann
Hélène Tourrière
Philippe Pasero
author_facet Julien N. Bianco
Valérie Bergoglio
Yea-Lih Lin
Marie-Jeanne Pillaire
Anne-Lyne Schmitz
Julia Gilhodes
Amelie Lusque
Julien Mazières
Magali Lacroix-Triki
Theodoros I. Roumeliotis
Jyoti Choudhary
Jérôme Moreaux
Jean-Sébastien Hoffmann
Hélène Tourrière
Philippe Pasero
author_sort Julien N. Bianco
title Overexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner
title_short Overexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner
title_full Overexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner
title_fullStr Overexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner
title_full_unstemmed Overexpression of Claspin and Timeless protects cancer cells from replication stress in a checkpoint-independent manner
title_sort overexpression of claspin and timeless protects cancer cells from replication stress in a checkpoint-independent manner
publisher Nature Portfolio
publishDate 2019
url https://doaj.org/article/fdf314771754477295f673e54990011e
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