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: | , , , , , , , , , , , , , , |
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Format: | article |
Language: | EN |
Published: |
Nature Portfolio
2019
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Subjects: | |
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. |
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