Processing of DNA structures via DNA unwinding and branch migration by the S. cerevisiae Mph1 protein.

[1]  S. Elledge,et al.  The DNA damage response: making it safe to play with knives. , 2010, Molecular cell.

[2]  S. Kowalczykowski,et al.  Rmi1 stimulates decatenation of double Holliday junctions during dissolution by Sgs1–Top3 , 2010, Nature Structural &Molecular Biology.

[3]  Rohit Prakash,et al.  Mechanism of the ATP-dependent DNA end-resection machinery from Saccharomyces cerevisiae , 2010, Nature.

[4]  A. D’Andrea,et al.  The FANCM/FAAP24 complex is required for the DNA interstrand crosslink-induced checkpoint response. , 2010, Molecular cell.

[5]  P. Sung,et al.  MHF1-MHF2, a histone-fold-containing protein complex, participates in the Fanconi anemia pathway via FANCM. , 2010, Molecular cell.

[6]  Weidong Wang,et al.  A histone-fold complex and FANCM form a conserved DNA-remodeling complex to maintain genome stability. , 2010, Molecular cell.

[7]  M. Whitby.  The FANCM family of DNA helicases/translocases. , 2010, DNA repair.

[8]  A. Constantinou,et al.  FANCM regulates DNA chain elongation and is stabilized by S‐phase checkpoint signalling , 2010, The EMBO journal.

[9]  R. Schwab,et al.  ATR activation and replication fork restart are defective in FANCM‐deficient cells , 2010, The EMBO journal.

[10]  Xiaolan Zhao,et al.  Interplay between the Smc5/6 complex and the Mph1 helicase in recombinational repair , 2009, Proceedings of the National Academy of Sciences.

[11]  L. Haracska,et al.  Role of Double-Stranded DNA Translocase Activity of Human HLTF in Replication of Damaged DNA , 2009, Molecular and Cellular Biology.

[12]  P. Sung,et al.  Functional significance of the Rad51-Srs2 complex in Rad51 presynaptic filament disruption , 2009, Nucleic acids research.

[13]  P. McGlynn,et al.  Replication fork reversal and the maintenance of genome stability , 2009, Nucleic acids research.

[14]  A. Constantinou,et al.  Remodeling of DNA replication structures by the branch point translocase FANCM , 2008, Proceedings of the National Academy of Sciences.

[15]  M. Whitby,et al.  The FANCM Ortholog Fml1 Promotes Recombination at Stalled Replication Forks and Limits Crossing Over during DNA Double-Strand Break Repair , 2008, Molecular cell.

[16]  Andrzej Stasiak,et al.  The Fanconi anemia protein FANCM can promote branch migration of Holliday junctions and replication forks. , 2008, Molecular cell.

[17]  L. Prakash,et al.  Yeast Rad5 Protein Required for Postreplication Repair Has a DNA Helicase Activity Specific for Replication Fork Regression , 2007, Molecular cell.

[18]  I. Hickson,et al.  The Bloom's Syndrome Helicase Can Promote the Regression of a Model Replication Fork* , 2006, Journal of Biological Chemistry.

[19]  C. Mathew,et al.  A human ortholog of archaeal DNA repair protein Hef is defective in Fanconi anemia complementation group M , 2005, Nature Genetics.

[20]  P. Sung,et al.  Saccharomyces cerevisiae MPH1 Gene, Required for Homologous Recombination-mediated Mutation Avoidance, Encodes a 3′ to 5′ DNA Helicase* , 2005, Journal of Biological Chemistry.

[21]  K. Komori,et al.  Cooperation of the N-terminal Helicase and C-terminal Endonuclease Activities of Archaeal Hef Protein in Processing Stalled Replication Forks* , 2004, Journal of Biological Chemistry.

[22]  Christian J. Rudolph,et al.  Yeast MPH1 gene functions in an error-free DNA damage bypass pathway that requires genes from Homologous recombination, but not from postreplicative repair. , 2004, Genetics.

[23]  Ying Li,et al.  DNA helicase Srs2 disrupts the Rad51 presynaptic filament , 2003, Nature.

[24]  F. Fabre,et al.  The Srs2 helicase prevents recombination by disrupting Rad51 nucleoprotein filaments , 2003, Nature.

[25]  Christian J. Rudolph,et al.  MPH1, a yeast gene encoding a DEAH protein, plays a role in protection of the genome from spontaneous and chemically induced damage. , 2000, Genetics.

[26]  J. Haber,et al.  Yeast Mph1 helicase dissociates Rad51-made D-loops: implications for crossover control in mitotic recombination. , 2009, Genes & development.