| Literature DB >> 8896563 |
J R Lo Ten Foe1, M A Rooimans, L Bosnoyan-Collins, N Alon, M Wijker, L Parker, J Lightfoot, M Carreau, D F Callen, A Savoia, N C Cheng, C G van Berkel, M H Strunk, J J Gille, G Pals, F A Kruyt, J C Pronk, F Arwert, M Buchwald, H Joenje.
Abstract
Fanconi anaemia (FA) is an autosomal recessive disorder characterized by a diversity of clinical symptoms including skeletal abnormalities, progressive bone marrow failure and a marked predisposition to cancer. FA cells exhibit chromosomal instability and hyper-responsiveness to the clastogenic and cytotoxic effects of bifunctional alkylating (cross-linking) agents, such as diepoxybutane (DEB) and mitomycin C (MMC). Five complementation groups (A-E) have been distinguished on the basis of somatic cell hybridization experiments, with group FA-A accounting for over 65% of the cases analysed. A cDNA for the group C gene (FAC) was reported and localized to chromosome 9q22.3 (ref.8). Genetic map positions were recently reported for two more FA genes, FAA (16q24.3) and FAD (3p22-26). Here we report the isolation of a cDNA representing the FAA gene, following an expression cloning method similar to the one used to clone the FAC gene. The 5.5-kb cDNA has an open reading frame of 4,368 nucleotides. In contrast to the 63-kD cytosolic protein encoded by the FAC gene, the predicted FAA protein (M(r) 162, 752) contains two overlapping bipartite nuclear localization signals and a partial leucine zipper consensus, which are suggestive of a nuclear localization.Entities:
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Year: 1996 PMID: 8896563 DOI: 10.1038/ng1196-320
Source DB: PubMed Journal: Nat Genet ISSN: 1061-4036 Impact factor: 38.330