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Cited by 311

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Expanded roles of the Fanconi anemia pathway in preserving genomic stability

Open access
Kee, Younghoon, D'Andrea, Alan D.·2010·Genes & Development

Abstract

Studying rare human genetic diseases often leads to a better understanding of normal cellular functions. Fanconi anemia (FA), for example, has elucidated a novel DNA repair mechanism required for maintaining genomic stability and preventing cancer. The FA pathway, an essential tumor-suppressive pathway, is required for protecting the human genome from a specific type of DNA damage; namely, DNA interstrand cross-links (ICLs). In this review, we discuss the recent progress in the study of the FA pathway, such as the identification of new FANCM-binding partners and the identification of RAD51C and FAN1 (Fanconi-associated nuclease 1) as new FA pathway-related proteins. We also focus on the role of the FA pathway as a potential regulator of DNA repair choices in response to double-strand breaks, and its novel functions during the mitotic phase of the cell cycle.

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Metadata

Authors
Kee, Y., & D'Andrea, A. D.
Venue
Genes & Development
Published
2010-08-15
Volume
24
Issue
16
Pages
1680-1694
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
OpenAlex
W2114776482
Cited by
311
References
18
Type
posted content
Language
en
Open access
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CoChat. (2026). Citation check: Expanded roles of the Fanconi anemia pathway in preserving genomic stability. https://app.cochat.ai/papers/10.1101/gad.1955310
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Kee, Y., & D'Andrea, A. D. (2010). Expanded roles of the Fanconi anemia pathway in preserving genomic stability. Genes & Development. https://doi.org/10.1101/gad.1955310

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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.