2019年5月24日 · Here we propose quantitative DSB sequencing (qDSB-Seq), a method providing both DSB frequencies per cell and their precise genomic coordinates. We induce spike-in DSBs by a site-specific...

2010年2月26日 · Hydroxyurea (HU) depletes the cells of dNTPs, which initially results in stalled replication forks that, after prolonged treatment, collapse into DSBs. Here, we report that stalled replication forks are efficiently restarted in a RAD51-dependent process that does not trigger homologous recombination (HR).

2022年12月26日 · Upon the occurrence of DNA double strand breaks (DSB), the proximal histone variant H2A.X is phosphorylated as γ-H2A.X, a critical signal for consequent DSB signaling and repair pathways.

2018年10月31日 · DNA double-strand breaks (DSBs) are one of the most lethal types of DNA lesions 1, being a primary source of chromosome translocations and deletions 2. Since DSBs...

2005年12月9日 · The topoisomerase inhibitor camptothecin (CPT) and dNTP synthesis-inhibitor hydroxyurea (HU) induce DSB by stalling DNA replication forks, whereas H 2 O 2 induces single-strand breaks (SSB). Cellular γ-H2AX, which increases after CPT or HU, but not H 2 O 2, treatment, is further increased in the presence of 25 nM OA (Figure 1 A).

2004年11月1日 · Using two different agents [ionizing radiation (IR) and hydroxyurea (HU)] to generate DSBs, we found that RPA relocated into distinct nuclear foci and colocalized with a well-known DSB binding factor, gamma-H2AX, at the sites of DNA damage in …

2023年7月20日 · 我们使用产生DNA双链断裂（DSB）的γ-照射（γ-IR），诱导单链断裂的喜树碱（CPT），氮芥（HN <2>），其产生链间交联（ICL），羟基脲（HU），其导致复制叉停止，从而防止DNA合成，和UV-C，其引起光产物（嘧啶二聚体）。 参见表1.在例如突变体与野生型相比，在各种DNA损伤剂中观察到的相对灵敏度/抗性之间的比较允许关于潜在修复途径受影响的推论。

2018年8月23日 · The END-seq DSB sites within 20 kb of each other were merged together using bedtools merge –d function. The resulting merged peaks were defined as the HU-DSB zones in the mouse samples. For HCT116 cells, only zones overlapping with at least two END-seq break-sites were retained.

2010年2月26日 · Hydroxyurea (HU) depletes the cells of dNTPs, which initially results in stalled replication forks that, after prolonged treatment, collapse into DSBs. Here, we report that stalled replication forks are efficiently restarted in a RAD51-dependent process that does not trigger homologous recombination (HR).

We devised a new methodology, Break-seq, that combines our previously described DSB labeling with next generation sequencing to map chromosome breaks with improved sensitivity and resolution. We show that DSBs preferentially occur at genes transcriptionally induced by HU.