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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Main Authors: 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
Format: article
Language:EN
Published: Nature Portfolio 2019
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Online Access:https://doaj.org/article/fdf314771754477295f673e54990011e
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Summary: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.