The Bloom's syndrome helicase suppresses crossing over during homologous recombination

By Leonard Wu, Ian D. Hickson. Nature, 2003

1,143 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/06a879e43e2c03a2a96c19369aea913d35d903c2

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Citations in the corpus

Playing the end game: DNA double-strand break repair pathway choice. (2012, background): “One mechanism involves BLM in complex with the topoisomerase TOPOIIIa, which promotes branch migration and topological decatenation of dHJ structures (dissolution) without crossover (Figure 4) (Wu and Hickson, 2003).”
Phosphorylation of BLM, Dissociation from Topoisomerase IIIα, and Colocalization with γ-H2AX after Topoisomerase I-Induced Replication Damage (2005, background): “The BLM-Top3 complex has been proposed to resolve stalled replication forks by resolution of recombination intermediates (double Holliday junctions) (35, 38, 68, 70, 72, 75).”
Homologous recombination and its regulation (2012, positive): “In addition, Sgs1– Top3–Rmi1 can dissolve dHJs in a non-crossover configuration; both Sgs1 and BLM promote the formation of hemicatenane structures by branch migrating two HJs between paired duplexes and this is followed by dissolution using topoisomerase III to produce non-crossover products (106,1”
Recombination proteins in yeast. (2004, background): “As a type IA topoisomerase, Topo III can make singlestranded incisions in ssDNA and catalyzes decatenation of negatively supercoiled plasmids.”
Regulation of homologous recombination in eukaryotes (2010, background): “This role of Sgs1 correlates with the ability of the human BLM-TOPO3alpha-RMI complex to dissolve dHJs into noncrossover products (165).”
DNA double-strand break repair: from mechanistic understanding to cancer treatment. (2007, background): “Nevertheless, it is important to point out that the human BLM and topoisomerase III proteins may resolve double Holliday Junctions to avoid cross-over products [54,63], which is consistent with the possibility that such double crossover intermediates indeed can form in mitotic cells.”
Maintaining genome stability at the replication fork (2010, background): “The sister chromatid junctions formed through template-switch processes are resolved by the action of the RecQ helicases Sgs1 (in yeast) and Bloom syndrome protein ( BLM ; in humans), together with the topoisomerase Top”
DNA interstrand crosslink repair and cancer (2011, neutral): “3 ), second end capture and extension will lead to the completion of replication and the formation of a double Holliday junction (DHJ) that can be dissolved by the BTR complex (comprised of the BLM RecQ helicase, topoisomerase IIIα (TOPOIIIα), RecQ-mediated genome instability 1 (RMI1) and RMI2) in a”
Hydroxyurea-Stalled Replication Forks Become Progressively Inactivated and Require Two Different RAD51-Mediated Pathways for Restart and Repair (2010, background): “Holliday Junction dissolution by the BLM-Top3 complex would dissolve any remaining double Holliday Junctions (Wu and Hickson, 2003).”
BLM-DNA2-RPA-MRN and EXO1-BLM-RPA-MRN constitute two DNA end resection machineries for human DNA break repair. (2011, background): “This phenotype is a consequence of two other activities of BLM helicase and its orthologs: disruption of DNA pairing intermediates (Harmon and Kowalczykowski 1998; Bugreev et al. 2007) and the dissolution of double Holliday junctions (Wu and Hickson 2003; Cejka et al. 2010b).”