recq helicases


Summary: A family of structurally-related DNA helicases that play an essential role in the maintenance of genome integrity. RecQ helicases were originally discovered in E COLI and are highly conserved across both prokaryotic and eukaryotic organisms. Genetic mutations that result in loss of RecQ helicase activity gives rise to disorders that are associated with CANCER predisposition and premature aging.

Top Publications

  1. Viziteu E, Klein B, Basbous J, Lin Y, Hirtz C, Gourzones C, et al. RECQ1 helicase is involved in replication stress survival and drug resistance in multiple myeloma. Leukemia. 2017;31:2104-2113 pubmed publisher
    ..b>RecQ helicases are DNA unwinding enzymes involved in the maintenance of chromosome stability...
  2. Chang E, Novoa C, Aristizabal M, Coulombe Y, Segovia R, Chaturvedi R, et al. RECQ-like helicases Sgs1 and BLM regulate R-loop-associated genome instability. J Cell Biol. 2017;216:3991-4005 pubmed publisher
    ..Together, our data describe a conserved role for Sgs1/BLM in R-loop suppression and support an increasingly broad view of DNA repair and replication fork stabilizing proteins as modulators of R-loop-mediated genome instability. ..
  3. Okoniewski S, Uyetake L, Perkins T. Force-activated DNA substrates for probing individual proteins interacting with single-stranded DNA. Nucleic Acids Res. 2017;45:10775-10782 pubmed publisher
    ..More broadly, these substrates enable the precise initiation of an important class of protein-DNA interactions. ..
  4. Sorenson K, Mahaney B, Lees Miller S, Cobb J. The non-homologous end-joining factor Nej1 inhibits resection mediated by Dna2-Sgs1 nuclease-helicase at DNA double strand breaks. J Biol Chem. 2017;292:14576-14586 pubmed publisher
  5. Woodrick J, Gupta S, Camacho S, Parvathaneni S, Choudhury S, Cheema A, et al. A new sub-pathway of long-patch base excision repair involving 5' gap formation. EMBO J. 2017;36:1605-1622 pubmed publisher
    ..Based on these results, we propose a revised model of long-patch BER and a new key regulation point for pathway choice in BER. ..
  6. Reddy S, Li B, Comai L. Processing of human telomeres by the Werner syndrome protein. Cell Cycle. 2010;9:3137-8 pubmed publisher
  7. Yu C, Oshima J, Wijsman E, Nakura J, Miki T, Piussan C, et al. Mutations in the consensus helicase domains of the Werner syndrome gene. Werner's Syndrome Collaborative Group. Am J Hum Genet. 1997;60:330-41 pubmed
    ..Also, the location of the mutations indicates that the presence or absence of the helicase domain does not influence the WS phenotype and suggests that WS is the result of complete loss of function of the WRN gene product. ..
  8. Beattie T, Lees Miller S. Unraveling the roles of WRN and DNA-PKcs at telomeres. Aging (Albany NY). 2010;2:257-8 pubmed
  9. Rogers C, Bochman M. Saccharomyces cerevisiae Hrq1 helicase activity is affected by the sequence but not the length of single-stranded DNA. Biochem Biophys Res Commun. 2017;486:1116-1121 pubmed publisher
    ..These results establish the importance of DNA sequence in Hrq1 helicase activity, and the absence of Hrq1 strand annealing activity explains the previously identified discrepancies between S. cerevisiae Hrq1 and human RecQ4. ..

More Information


  1. Di Marco S, Hasanova Z, Kanagaraj R, Chappidi N, Altmannova V, Menon S, et al. RECQ5 Helicase Cooperates with MUS81 Endonuclease in Processing Stalled Replication Forks at Common Fragile Sites during Mitosis. Mol Cell. 2017;66:658-671.e8 pubmed publisher
    ..These data suggest that RECQ5 removes RAD51 filaments stabilizing stalled replication forks at CFSs and hence facilitates CFS cleavage by MUS81-EME1. ..
  2. Hoadley K, Keck J. Werner helicase wings DNA binding. Structure. 2010;18:149-51 pubmed publisher
    ..describe the structure of the DNA-bound winged-helix domain from the Werner helicase. This structure of a RecQ/DNA complex offers insights into the DNA-unwinding mechanisms of RecQ family helicases. ..
  3. Wang J, Chen J, Gong Z. TopBP1 stabilizes BLM protein to suppress sister chromatid exchange. Mol Cell. 2015;57:955-956 pubmed publisher
  4. Brunauer R, Kennedy B. Medicine. Progeria accelerates adult stem cell aging. Science. 2015;348:1093-4 pubmed publisher
  5. West S, Blanco M, Chan Y, Matos J, Sarbajna S, Wyatt H. Resolution of Recombination Intermediates: Mechanisms and Regulation. Cold Spring Harb Symp Quant Biol. 2015;80:103-9 pubmed publisher
    ..The temporal regulation of the dissolution/resolution pathways is therefore critical for crossover avoidance while also ensuring that all covalent links between chromosomes are resolved before chromosome segregation. ..
  6. Li L, Poon H, Hildebrandt M, Monckton E, Germain D, Fahlman R, et al. Role for RIF1-interacting partner DDX1 in BLM recruitment to DNA double-strand breaks. DNA Repair (Amst). 2017;55:47-63 pubmed publisher
  7. Guo X, Hum Y, Lehner K, Jinks Robertson S. Regulation of hetDNA Length during Mitotic Double-Strand Break Repair in Yeast. Mol Cell. 2017;67:539-549.e4 pubmed publisher
    ..Data are most consistent with the extent of DNA synthesis from the invading end being the primary determinant of hetDNA length during SDSA. ..
  8. Sobinoff A, Allen J, Neumann A, Yang S, Walsh M, Henson J, et al. BLM and SLX4 play opposing roles in recombination-dependent replication at human telomeres. EMBO J. 2017;36:2907-2919 pubmed publisher
    ..Our data are consistent with ALT being a conservative DNA replication process, analogous to break-induced replication, which is dependent on BTR and counteracted by SLX4 complex-mediated resolution events. ..
  9. Legerski R. The Pso4 complex splices into the DNA damage response. Cell Cycle. 2009;8:3448-9 pubmed
  10. Chan K, Hickson I. On the origins of ultra-fine anaphase bridges. Cell Cycle. 2009;8:3065-6 pubmed