Abstract
We have identified three novel FANCC mutations, a truncating single base insertion in exon 4 (c.455_456dupA), a point mutation in exon 13 (c.1390C>T), and a splice site mutation leading to deletion of exon 9, in two Brazilian FA-C patients, each a compound heterozygote. Using complementation analyses, we confirmed that two of these mutations inactivate the function of the FANCC protein.
2006 Wiley-Liss, Inc.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Bone Marrow Cells / cytology
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Brazil
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Child
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DNA Mutational Analysis
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Exons
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Fanconi Anemia Complementation Group C Protein / genetics*
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Female
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Gene Deletion
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Genetic Complementation Test
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Humans
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Mutation*
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RNA Splicing
Substances
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Fanconi Anemia Complementation Group C Protein