Expanded roles of the Fanconi anemia pathway in preserving genomic stability
- 15 August 2010
- journal article
- review article
- Published by Cold Spring Harbor Laboratory in Genes & Development
- Vol. 24 (16), 1680-1694
- https://doi.org/10.1101/gad.1955310
Abstract
Studying rare human genetic diseases often leads to a better understanding of normal cellular functions. Fanconi anemia (FA), for example, has elucidated a novel DNA repair mechanism required for maintaining genomic stability and preventing cancer. The FA pathway, an essential tumor-suppressive pathway, is required for protecting the human genome from a specific type of DNA damage; namely, DNA interstrand cross-links (ICLs). In this review, we discuss the recent progress in the study of the FA pathway, such as the identification of new FANCM-binding partners and the identification of RAD51C and FAN1 (Fanconi-associated nuclease 1) as new FA pathway-related proteins. We also focus on the role of the FA pathway as a potential regulator of DNA repair choices in response to double-strand breaks, and its novel functions during the mitotic phase of the cell cycle.Keywords
This publication has 123 references indexed in Scilit:
- A Genetic Screen Identifies FAN1, a Fanconi Anemia-Associated Nuclease Necessary for DNA Interstrand Crosslink RepairMolecular Cell, 2010
- 53BP1 Inhibits Homologous Recombination in Brca1-Deficient Cells by Blocking Resection of DNA BreaksCell, 2010
- A Selective Requirement for 53BP1 in the Biological Response to Genomic Instability Induced by Brca1 DeficiencyMolecular Cell, 2009
- FANCM–FAAP24 and FANCJ: FA proteins that metabolize DNAMutation Research - Reviews in Mutation Research, 2009
- PALB2 Links BRCA1 and BRCA2 in the DNA-Damage ResponseCurrent Biology, 2009
- Inactivation of Murine Usp1 Results in Genomic Instability and a Fanconi Anemia PhenotypeDevelopmental Cell, 2009
- The FANCM Ortholog Fml1 Promotes Recombination at Stalled Replication Forks and Limits Crossing Over during DNA Double-Strand Break RepairMolecular Cell, 2008
- Deubiquitination of FANCD2 Is Required for DNA Crosslink RepairMolecular Cell, 2007
- Double-strand breaks induce homologous recombinational repair of interstrand cross-links via cooperation of MSH2, ERCC1-XPF, REV3, and the Fanconi anemia pathwayDNA Repair, 2007
- Identification of the FANCI Protein, a Monoubiquitinated FANCD2 Paralog Required for DNA RepairCell, 2007