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Cited by 1,322

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Linkage of ATM to Cell Cycle Regulation by the Chk2 Protein Kinase

Matsuoka, S.·1998·Science

Abstract

In response to DNA damage and replication blocks, cells prevent cell cycle progression through the control of critical cell cycle regulators. We identified Chk2, the mammalian homolog of the Saccharomyces cerevisiae Rad53 and Schizosaccharomyces pombe Cds1 protein kinases required for the DNA damage and replication checkpoints. Chk2 was rapidly phosphorylated and activated in response to replication blocks and DNA damage; the response to DNA damage occurred in an ataxia telangiectasia mutated (ATM)-dependent manner. In vitro, Chk2 phosphorylated Cdc25C on serine-216, a site known to be involved in negative regulation of Cdc25C. This is the same site phosphorylated by the protein kinase Chk1, which suggests that, in response to DNA damage and DNA replicational stress, Chk1 and Chk2 may phosphorylate Cdc25C to prevent entry into mitosis.

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Metadata

Authors
Matsuoka, S.
Venue
Science
Published
1998-12-04
Volume
282
Issue
5395
Pages
1893-1897
ISSN
0036-8075 (ISSN-L)
OpenAlex
W1988876917
Cited by
1,322
References
5
FWCI
27.80
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Linkage of ATM to Cell Cycle Regulation by the Chk2 Protein Kinase. https://app.cochat.ai/papers/10.1126/science.282.5395.1893
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Matsuoka, S. (1998). Linkage of ATM to Cell Cycle Regulation by the Chk2 Protein Kinase. Science. https://doi.org/10.1126/science.282.5395.1893

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.