Buscar
Mostrando ítems 1-5 de 5
Artículo
Homologous recombination repairs secondary replication induced DNA double-strand breaks after ionizing radiation
(Oxford University Press, 2012)
Ionizing radiation (IR) produces direct two-ended DNA double-strand breaks (DSBs) primarily repaired by non-homologous end joining (NHEJ). It is, however, well established that homologous recombination (HR) is induced and ...
Artículo
The PARP inhibitor Olaparib disrupts base excision repair of 5-aza-2′-deoxycytidine lesions
(Oxford University Press, 2014)
Decitabine (5-aza-21-deoxycytidine, 5-azadC) is used in the treatment of Myelodysplatic syndrome (MDS) and Acute Myeloid Leukemia (AML). Its mechanism of action is thought to involve reactivation of genes implicated in ...
Artículo
Hydroxyurea-Stalled Replication Forks Become Progressively Inactivated and Require Two Different RAD51-Mediated Pathways for Restart and Repair
(Elsevier, 2010)
Faithful DNA replication is essential to all life. Hydroxyurea (HU) depletes the cells of dNTPs, which initially results in stalled replication forks that, after prolonged treatment, collapse into DSBs. Here, we report ...
Artículo
Zebularine induces replication-dependent double-strand breaks which are preferentially repaired by homologous recombination
(Elsevier, 2017)
Zebularine is a second-generation, highly stable hydrophilic inhibitor of DNA methylation with oral bioavailability that preferentially target cancer cells. It acts primarily as a trap for DNA methyl transferases (DNMTs) ...
Artículo
5-Aza-2'-deoxycytidine causes replication lesions that require Fanconi anemia-dependent homologous recombination for repair
(Oxford University Press, 2013)
5-Aza-2'-deoxycytidine (5-azadC) is a DNA methyltransferase (DNMT) inhibitor increasingly used in treatments of hematological diseases and works by being incorporated into DNA and trapping DNMT. It is unclear what DNA ...