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Fanconi anaemia proteins: Major roles in cell protection against oxidative damage
Italian National Cancer Institute, G. Pascale Foundation, Paediatric Oncology Research Centre, Mercogliano (AV), Italy, Istituto Nazionale Tumori, Fondazione G. Pascale, v. M. Semmola, I-80131 Naples, Italy.
Clinical Discovery, Bristol-Myers Squibb Company, Princeton, NJ, United States.
Dept. of Paediat. Haematol./Oncolog., Istanbul Univ. School of Medicine, Istanbul, Turkey.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Pharmacology .
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2003 (English)In: Bioessays, ISSN 0265-9247, Vol. 25, no 6, 589-595 p.Article, review/survey (Refereed) Published
Abstract [en]

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). © 2003 Wiley Periodicals, Inc.

Place, publisher, year, edition, pages
2003. Vol. 25, no 6, 589-595 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-46616DOI: 10.1002/bies.10283OAI: diva2:267512
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2011-01-13

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