RecQ helicases: caretakers of the genome

By Ian D. Hickson. Nature Reviews. Cancer, 2003

695 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/dc29ff73256716fa95509a5f8df8eb39d11e6a2e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Manel Esteller
2. H. Klein
3. P. Sung
4. Leonard Wu
5. Yves Pommier

In Molecular Biology

1. Y. Kubota
2. Manel Esteller
3. H. Klein
4. P. Sung
5. Yves Pommier
6. Leonard Wu
7. H. Takisawa
8. Ian D. Hickson

Citations in the corpus

• Phosphorylation of BLM, Dissociation from Topoisomerase IIIα, and Colocalization with γ-H2AX after Topoisomerase I-Induced Replication Damage (2005, background): “The causative gene of the cancer-predisposing genetic disease Bloom’s syndrome, BLM, is a member of the RecQ family of DNA helicases (28).”
• The Bloom's syndrome helicase suppresses crossing over during homologous recombination (2003, background): “, through the suppression of ectopic recombination and crossing over between homologous chromosome”
• Mechanism of homologous recombination: mediators and helicases take on regulatory functions (2006, background): “Several cancer-prone genetic diseases, including Bloom's syndrome and Fanconi anaemia , are associated with HR dysfunction or deficienc”
• The N-Terminal Noncatalytic Region of Xenopus RecQ4 Is Required for Chromatin Binding of DNA Polymerase α in the Initiation of DNA Replication (2006, background): “The region is required for the initiation of DNA replication, in particular for chromatin binding of DNA polymerase . In humans, mutations in RecQ4 are responsible for some cases of Rothmund-Thomson syndrome (2, 16, 20), suggesting that RecQ4 is important for preventing genome instability and that m”
• Epigenetic gene silencing in cancer: the DNA hypermethylome. (2007, background): “It has been suggested that RecQ family proteins act as tumor suppressors (92), and we demonstrated for the first time that the WRN gene undergoes epigenetic inactivation by CpG island promoter hypermethylation in various tumor types of both mesenchymal and epithelial origin, including those commonly”