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Cited by 528

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Phosphorylation of SMC1 is a critical downstream event in the ATM–NBS1–BRCA1 pathway

Open access
Kitagawa, Risa, Bakkenist, Christopher J., McKinnon, Peter J., Kastan, Michael B.·2004·Genes & Development

Abstract

The ATM protein kinase is activated by intermolecular autophosphorylation in response to DNA damage and initiates cellular signaling pathways that facilitate cell survival and reduce chromosomal breakage. Here, we show that NBS1 and BRCA1 are required for the recruitment of previously activated ATM to the sites of DNA breaks after ionizing irradiation, and that this recruitment is required for the phosphorylation of SMC1 by ATM. To explore the functional importance of SMC1 phosphorylation, murine cells were generated, in which the two damage-induced phosphorylation sites in SMC1 are mutated. Although these cells demonstrate normal phosphorylation and focus formation of ATM, NBS1, and BRCA1 proteins after IR, they exhibit a defective S-phase checkpoint, decreased survival, and increased chromosomal aberrations after DNA damage. These observations suggest that many of the abnormal stress responses seen in cells lacking ATM, NBS1, or BRCA1 result from a failure of ATM migration to sites of DNA breaks and a resultant lack of SMC1 phosphorylation.

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Metadata

Authors
Kitagawa, R., Bakkenist, C. J., McKinnon, P. J., & Kastan, M. B.
Venue
Genes & Development
Published
2004-06-02
Volume
18
Issue
12
Pages
1423-1438
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
OpenAlex
W2148172964
Cited by
528
References
6
Type
posted content
Language
en
Open access
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CoChat. (2026). Citation check: Phosphorylation of SMC1 is a critical downstream event in the ATM–NBS1–BRCA1 pathway. https://app.cochat.ai/papers/10.1101/gad.1200304
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Kitagawa, R., Bakkenist, C. J., McKinnon, P. J., & Kastan, M. B. (2004). Phosphorylation of SMC1 is a critical downstream event in the ATM–NBS1–BRCA1 pathway. Genes & Development. https://doi.org/10.1101/gad.1200304

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