Evidence for at least four Fanconi anaemia genes including FACC on chromosome 9
Copyright policy )Evidence for at least four Fanconi anaemia genes including FACC on chromosome 9
Fanconi anaemia (FA) is a DNA repair disorder characterized by cellular hypersensitivity to DNA cross-linking agents and extensive phenotypic heterogeneity. To determine the extent of genetic heterogeneity present in FA, a panel of somatic cell hybrids was constructed using polyethylene glycol-mediated cell fusion. Three new complementation groups were identified, designated FA(B), FA(C) and FA(D), and the gene defective in FA(C) which we have recently cloned was localized to chromosome 9q22.3 through in situ hybridization. These results suggest that mutations in at least four different genes lead to FA, a degree of genetic heterogeneity comparable to that of other DNA repair disorders.
- University of Toronto Canada
- Queen's University Canada
- Kingston General Hospital Canada
- Hospital for Sick Children Canada
Genetic Markers, Fanconi Anemia, DNA Repair, Genetic Complementation Test, Chromosome Mapping, Humans, Hybrid Cells, Chromosomes, Human, Pair 9, In Situ Hybridization
Genetic Markers, Fanconi Anemia, DNA Repair, Genetic Complementation Test, Chromosome Mapping, Humans, Hybrid Cells, Chromosomes, Human, Pair 9, In Situ Hybridization
citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).335 popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.Top 10% influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).Top 1% impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.Top 1%
Citations provided by BIP!Popularity provided by BIP!