Fanconi anaemia proteins: Major roles in cell protection against oxidative damage

Giovanni Pagano, Hagop Youssoufian, Sema S. Anak, Ulf T. Brunk, Rita Calzone, Alan A. Clarke, Paolo Degan, Marco D'Ischia, Christina Dunster, Aldo Giudice, Mario Iaccarino, Monica Hirsch-Kauffmann, Frank J. Kelly, Ana Lloret, Walter Malorni, Paola Manini, Roberta Masella, Bruno Nobili, Federico V. Pallardó, Manfred SchweigerEmilia Vuttariello, Garo Youssoufian, Adriana Zatterale

Research output: Contribution to journalArticlepeer-review


Fanconi anaemia (FA) is a cancer-prone genetic disorder that is characterised by cytogenetic instability and redox abnormalities. Although rare subtypes of FA (B, D1 and D2) have been implicated in DNA repair through links with BRCA1 and BRCA2, such a role has yet to be demonstrated for gene products of the common subtypes. Instead, these products have been strongly implicated in xenobiotic metabolism and redox homeostasis through interactions of FANCC with cytochrome P-450 reductase and with glutathione S-transferase, and of FANCG with cytochrome P-450 2E1, as well as redox-dependent signalling through an interaction between FANCA and Akt kinase. We hypothesise that FA proteins act directly (via FANCC and FANCG) and indirectly (via FANCA, BRCA2 and FANCD2) with the machinery of cellular defence to modulate oxidative stress. The latter interactions may co-ordinate the link between the response to DNA damage and oxidative stress parameters (3, 6-12).

Original languageEnglish
Pages (from-to)589-595
Number of pages7
Issue number6
Publication statusPublished - Jun 1 2003

ASJC Scopus subject areas

  • Neuroscience (miscellaneous)
  • Biochemistry
  • Cell Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Developmental Biology
  • Agricultural and Biological Sciences (miscellaneous)
  • Plant Science


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