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Open AccessJournal ArticleDOI

Proteome dynamics at broken replication forks reveal a distinct ATM-directed repair response suppressing DNA double-strand break ubiquitination

TLDR
In this article, the authors used nascent chromatin capture (NCC) proteomics to characterize the repair of replication-associated DNA double-strand breaks (DSBs) triggered by topoisomerase 1 (TOP1) inhibitors.
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This article is published in Molecular Cell.The article was published on 2021-03-04 and is currently open access. It has received 37 citations till now. The article focuses on the topics: DNA repair & DNA replication.

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Human topoisomerases and their roles in genome stability and organization

TL;DR: Topoisomerases are a family of six enzymes: TOP1 and TOP1MT, TOP2A and TOP2B, and two types IA and TOP3A as discussed by the authors .
Journal ArticleDOI

Cellular functions of the protein kinase ATM and their relevance to human disease.

TL;DR: The protein kinase ataxia telangiectasia mutated (ATM) is a master regulator of double-strand DNA break (DSB) signalling and stress responses as discussed by the authors.
Journal ArticleDOI

Hallmarks of DNA replication stress.

Sneha Saxena, +1 more
- 01 Jun 2022 - 
TL;DR: A review on the major sources of replication stress, the impacts of DNA replication stress in cells, and the assays to detect replication stress can be found in this paper , which provides an overview of the hallmarks of the replication stress.
Journal ArticleDOI

Present and Future Perspective on PLK1 Inhibition in Cancer Treatment

TL;DR: The evidence suggesting the role of PLK1 in response to DNA damage, including DNA repair, cell cycle progression, epithelial to mesenchymal transition, cell death pathways and cancer-related immunity is summarized.
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Journal Article

Arrest of Replication Forks by Drug-stabilized Topoisomerase I-DNA Cleavable Complexes as a Mechanism of Cell Killing by Camptothecin

TL;DR: It is proposed that the collision between moving replication forks and camptothecin-stabilized topoisomerase I-DNA cleavable complexes results in fork arrest and possibly fork breakage, which are lethal to proliferating cells.
Journal ArticleDOI

Orchestration of the DNA-Damage Response by the RNF8 Ubiquitin Ligase

TL;DR: The results demonstrate how the DNA-damage response is orchestrated by ATM-dependent phosphorylation of MDC1 and RNF8-mediated ubiquitination and promote the G2/M DNA damage checkpoint and resistance to ionizing radiation.
Journal ArticleDOI

Hydroxyurea-Stalled Replication Forks Become Progressively Inactivated and Require Two Different RAD51-Mediated Pathways for Restart and Repair

TL;DR: The XRCC3 protein, which is required for RAD51 foci formation, is also required for replication restart of HU-stalled forks, suggesting that RAD51-mediated strand invasion supports fork restart.
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Abraxas and RAP80 Form a BRCA1 Protein Complex Required for the DNA Damage Response

TL;DR: Phosphopeptide affinity proteomic analysis identified a protein, Abraxas, that directly binds the BRCA1 BRCT repeats through a phospho-Ser-X- X-Phe motif, forming a third type of B RCA1 complex.
Journal ArticleDOI

RAP80 targets BRCA1 to specific ubiquitin structures at DNA damage sites.

TL;DR: Mutations affecting the BRCT domains of the breast cancer–associated tumor suppressor BRCA1 disrupt the recruitment of this protein to DNA double-strand breaks (DSBs), implicating ubiquitin chain recognition and turnover in the BRCa1-mediated repair of DSBs.
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