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Cited by 408

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ATR couples FANCD2 monoubiquitination to the DNA-damage response

Open access
Andreassen, Paul R., D'Andrea, Alan D., Taniguchi, Toshiyasu·2004·Genes & Development

Abstract

Fanconi anemia (FA) is a multigenic autosomal recessive cancer susceptibility syndrome. The FA pathway regulates the monoubiquitination of FANCD2 and the assembly of damage-associated FANCD2 nuclear foci. How FANCD2 monoubiquitination is coupled to the DNA-damage response has remained undetermined. Here, we demonstrate that the ATR checkpoint kinase and RPA1 are required for efficient FANCD2 monoubiquitination. Deficiency of ATR function, either in Seckel syndrome, which clinically resembles Fanconi anemia, or by siRNA silencing, results in the formation of radial chromosomes in response to the DNA cross-linker, mitomycin C (MMC), thus mimicking the chromosome instability of FA cells.

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Metadata

Authors
Andreassen, P. R., D'Andrea, A. D., & Taniguchi, T.
Venue
Genes & Development
Published
2004-08-15
Volume
18
Issue
16
Pages
1958-1963
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
OpenAlex
W2142544392
Cited by
408
References
5
Type
posted content
Language
en
Open access
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CoChat. (2026). Citation check: ATR couples FANCD2 monoubiquitination to the DNA-damage response. https://app.cochat.ai/papers/10.1101/gad.1196104
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Andreassen, P. R., D'Andrea, A. D., & Taniguchi, T. (2004). ATR couples FANCD2 monoubiquitination to the DNA-damage response. Genes & Development. https://doi.org/10.1101/gad.1196104

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