Fanconi anaemia proteins are associated with sister chromatid bridging in mitosis

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• 作者：Songmin Ying (1)
  Ian D. Hickson (1) (2)
  
• 关键词：Bloom’s syndrome ; Fanconi anaemia ; DNA replication ; Anaphase bridges ; Common fragile sites
• 刊名：International Journal of Hematology
• 出版年：2011
• 出版时间：April 2011
• 年：2011
• 卷：93
• 期：4
• 页码：440-445
• 全文大小：211KB
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• 作者单位：Songmin Ying (1)
  Ian D. Hickson (1) (2)
  
  1. Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, OX39DS, UK
  2. Department of Cellular and Molecular Medicine, Center for Healthy Aging, Panum Institute, University of Copenhagen, Blegdamsvej 3B, Building 18.1.32, 2200, Copenhagen N, Denmark
  

文摘

The maintenance of genome stability is critical for the suppression of cancer and premature ageing. The maintenance of the human genome requires hundreds of proteins involved in DNA repair, DNA replication, chromosome segregation and cell cycle checkpoint responses. A number of genetic disorders exist in man where a breakdown in genome maintenance is associated with cancer predisposition. Amongst these are Bloom’s syndrome (BS) and Fanconi anaemia (FA). The BS and FA gene products co-operate in the repair of damaged DNA. In this review, we focus on interactions between BS and FA proteins that specifically occur during chromosome segregation in mitosis. The BS protein, BLM, was shown recently to define a novel class of anaphase DNA bridge structures that, in some cases, also contain FA proteins. We will discuss the possible source of these bridges and the role that FA proteins and BLM might play in their removal.