ArticleAmerican journal of human genetics2000
Localization of the Fanconi anemia complementation group D gene to a 200-kb region on chromosome 3p25.3.
Article in American journal of human genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Immunohistochemical analysis of p53 in vulval intraepithelial neoplasia and vulval squamous cell carcinoma.British journal of cancer · 2003Pooled it
- The Fanconi anemia ID2 complex: dueling saxes at the crossroads.Cell cycle (Georgetown, Tex.) · 2014Review
- AMD3100 synergizes with G-CSF to mobilize repopulating stem cells in Fanconi anemia knockout mice.Experimental hematology · 2008Article
- Tip60 is required for DNA interstrand cross-link repair in the Fanconi anemia pathway.The Journal of biological chemistry · 2008Article
- FANCG is phosphorylated at serines 383 and 387 during mitosis.Molecular and cellular biology · 2004Article
- Fanconi anemia in Tunisia: high prevalence of group A and identification of new FANCA mutations.Journal of human genetics · 2003Article
- Molecular pathogenesis of fanconi anemia.International journal of hematology · 2002Review
- Current knowledge on the pathophysiology of Fanconi anemia: from genes to phenotypes.International journal of hematology · 2001Review
- Isolation of a cDNA representing the Fanconi anemia complementation group E gene.American journal of human genetics · 2000Article
- A never-ending story: the steadily growing family of the FA and FA-like genes.Genetics and molecular biologyArticle
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Authors and funding
15 authors at 2 institutions in 1 country.
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Abstract
Fanconi anemia (FA) is a rare autosomal recessive disease manifested by bone-marrow failure and an elevated incidence of cancer. Cells taken from patients exhibit spontaneous chromosomal breaks and rearrangements. These breaks and rearrangements are greatly elevated by treatment of FA cells with the use of DNA cross-linking agents. The FA complementation group D gene (FANCD) has previously been localized to chromosome 3p22-26, by use of microcell-mediated chromosome transfer. Here we describe the use of noncomplemented microcell hybrids to identify small overlapping deletions that narrow the FANCD critical region. A 1.2-Mb bacterial-artificial-chromosome (BAC)/P1 contig was constructed, bounded by the marker D3S3691 distally and by the gene ATP2B2 proximally. The contig contains at least 36 genes, including the oxytocin receptor (OXTR), hOGG1, the von Hippel-Lindau tumor-suppressor gene (VHL), and IRAK-2. Both hOGG1 and IRAK-2 were excluded as candidates for FANCD. BACs were then used as probes for FISH analyses, to map the extent of the deletions in four of the noncomplemented microcell hybrid cell lines. A narrow region of common overlapping deletions limits the FANCD critical region to approximately 200 kb. The three candidate genes in this region are TIGR-A004X28, SGC34603, and AA609512.
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