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Nature 456, 453-454 (27 November 2008) | doi:10.1038/456453a; Published online 26 November 2008
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Molecular biology: The Bloom's complex mousetrap
Robert M. Brosh, Jr1
Abstract
Genomic instability often underlies cancer. Analyses of proteins implicated in a cancer-predisposing condition called Bloom's syndrome illustrate the intricacies of protein interactions that ensure genomic stability.
Bloom's syndrome, which is characterized by severe growth retardation, immunodeficiency, anaemia, reduced fertility and predisposition to cancer1, is caused by mutations in the gene BLM. At the cellular level, the hallmark of this genetic disorder is a high rate of sister-chromatid exchange — the swapping of homologous stretches of DNA between a chromosome and its identical copy generated during DNA replication2.
- Robert M. Brosh Jr is in the Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, NIH Biomedical Research Center, Baltimore, Maryland 21224, USA.
Email: broshr@mail.nih.gov
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NEWS AND VIEWS
A new deal for Holliday junctionsNature Structural & Molecular Biology News and Views (01 Feb 2004)
RESEARCH
BLAP75, an essential component of Bloom's syndrome protein complexes that maintain genome integrityThe EMBO Journal Article (06 Apr 2005)
BLM and the FANC proteins collaborate in a common pathway in response to stalled replication forksThe EMBO Journal Article (04 Aug 2004)
The HRDC domain of BLM is required for the dissolution of double Holliday junctionsThe EMBO Journal Article (20 Jul 2005)
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