BCR/ABL stimulates WRN to promote survival and genomic instability.

BCR/ABL-transformed chronic myeloid leukemia (CML) cells accumulate numerous DNA double-strand breaks (DSB) induced by reactive oxygen species (ROS) and genotoxic agents. To repair these lesions BCR/ABL stimulate unfaithful DSB repair pathways, homologous recombination repair (HRR), nonhomologous end-joining (NHEJ), and single-strand annealing (SSA). Here, we show that BCR/ABL enhances the expression and increase nuclear localization of WRN (mutated in Werner syndrome), which is required for processing DSB ends during the repair.

[Role of oxidative mechanisms in the pathogenesis of age-related macular degeneration].

Oxidative stress is a major factor in the pathogenesis of age-related macular degeneration (AMD). Retinal pigment epithelial (RPE) cells are prone to reactive oxygen species (ROS) arising during the stress due to intense oxygen metabolism and a high oxygen pressure. Additionally, the cells can be exposed to ROS as a consequence of accumulation of iron ions in these cells, sunlight exposure and tobacco smoke.

[Non-homologous DNA end joining--new proteins, new functions, new mechanisms].

Humans use primarily nonhomologous end joining (NHEJ) to repair DNA double strand breaks (DSBs), which are the most serious DNA damage, resulting in cell death if non-repaired or missrepaired. NHEJ directly joins together DNA ends resulted from DSBs. This pathway plays a key role in the development of vertebrate immune system through its involvement in the V(D)J recombination.