ArticleProceedings of the National Academy of Sciences of the United States of America1992
Elevated sister chromatid exchange phenotype of Bloom syndrome cells is complemented by human chromosome 15.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Moving Beyond Somatic Alterations: Uncovering the Germline Basis of Myeloid Malignancies.Cancers · 2026Review
- Intellectual disability and abnormal cortical neuron phenotypes in patients with Bloom syndrome.Journal of human genetics · 2023Article
- DEAD/H-Box Helicases in Immunity, Inflammation, Cell Differentiation, and Cell Death and Disease.Cells · 2022Review
- Bloom's Syndrome: Clinical Spectrum, Molecular Pathogenesis, and Cancer Predisposition.Molecular syndromology · 2017Review
- The BLM dissolvasome in DNA replication and repair.Cellular and molecular life sciences : CMLS · 2013Review
- DNA replication arrest leads to enhanced homologous recombination and cell death in meristems of rice OsRecQl4 mutants.BMC plant biology · 2013Article
- On BLM helicase in recombination-mediated telomere maintenance.Molecular biology reports · 2013Article
- The manipulation of chromosomes by mankind: the uses of microcell-mediated chromosome transfer.Chromosoma · 2005Review
- Mapping of a single locus capable of complementing the defective heterochromatin phenotype of Roberts syndrome cells.American journal of human genetics · 2005Article
- RecQ helicases: suppressors of tumorigenesis and premature aging.The Biochemical journal · 2003Review
- Microcell-mediated chromosome transfer (MMCT): small cells with huge potential.Mammalian genome : official journal of the International Mammalian Genome Society · 2003Review
- Bloom's syndrome protein is required for correct relocalization of RAD50/MRE11/NBS1 complex after replication fork arrest.The Journal of cell biology · 2002Article
- Transfection of BLM into cultured bloom syndrome cells reduces the sister-chromatid exchange rate toward normal.American journal of human genetics · 1999Article
- Chromosome breakage in the Prader-Willi and Angelman syndromes involves recombination between large, transcribed repeats at proximal and distal breakpoints.American journal of human genetics · 1999Article
- A model system to study genomic imprinting of human genes.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Gene structure, DNA methylation, and imprinted expression of the human SNRPN gene.American journal of human genetics · 1996Article
- Characterization of the XRCC1-DNA ligase III complex in vitro and its absence from mutant hamster cells.Nucleic acids research · 1995Article
- Low-sister-chromatid-exchange Bloom syndrome cell lines: an important new tool for mapping the basic genetic defect in Bloom syndrome and for unraveling the biology of human tumor development.American journal of human genetics · 1995Article
- Mammalian DNA ligase III: molecular cloning, chromosomal localization, and expression in spermatocytes undergoing meiotic recombination.Molecular and cellular biology · 1995Article
- The human RAD51/RecA homologue gene is not a candidate gene for Bloom's syndrome.Human genetics · 1994Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Bloom syndrome (BSx) is a rare autosomal-recessive chromosome-instability disorder manifested by a constellation of clinical features including a significant predisposition to early onset of neoplasia. BSx cells display cytogenetic abnormalities, the pathognomonic feature being an increased rate of spontaneous sister chromatid exchanges (SCEs), 10- to 15-fold more frequent than SCEs seen in control cells. Identification of the primary biochemical defect in BSx and its relationship to SCE frequency and neoplasia have been complicated by reports that BSx cell lines exhibit defects in the structure and/or activity of a number of different enzymes. The rare occurrence of the disorder and lack of informative families have precluded mapping of the primary defect by standard linkage analysis. We have utilized BSx cells as recipients for microcell-mediated chromosome transfer to map a locus that renders complementation of the elevated SCE phenotype. Studies with the BSx cell line GM08505 demonstrated a stable frequency of SCEs 10-fold higher than control values, offering a phenotype suitable for complementation studies. Transfer of different independent human chromosomes from somatic cell hybrids into BSx cells permitted identification of a single chromosome that dramatically reduced the SCE frequency to a level near that seen in control cells. Detailed characterization revealed this complementing element to be human chromosome 15.
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