Proteome dynamics at broken replication forks reveal a distinct ATM-directed repair response suppressing DNA double-strand break ubiquitination
Kyosuke Nakamura,Georg Kustatscher,Constance Alabert,Martina Hödl,Ignasi Forné,Moritz Völker-Albert,Shankha Satpathy,Tracey E. Beyer,Niels Mailand,Chunaram Choudhary,Axel Imhof,Juri Rappsilber,Juri Rappsilber,Anja Groth +13 more
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.About:
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.read more
Citations
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Talazoparib monotherapy in metastatic castration-resistant prostate cancer with DNA repair alterations (TALAPRO-1): an open-label, phase 2 trial
Johann S. de Bono,Niven Mehra,Giorgio V. Scagliotti,Elena Castro,Tanya B. Dorff,A. Stirling,Arnulf Stenzl,Mark D. Fleming,Celestia S. Higano,Fred Saad,Consuelo Buttigliero,Inge M. van Oort,A. Douglas Laird,Marielena Mata,Hsiang-Chun Chen,Cynthia G. Healy,Akos Czibere,Karim Fizazi +17 more
TL;DR: In this paper, the authors assessed the PARP inhibitor talazoparib in metastatic castration-resistant prostate cancers with DNA damage response (DDR) alterations in genes involved directly or indirectly in homologous recombination repair (HRR).
Journal ArticleDOI
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.
Ji-Hoon Lee,Tanya T. Paull +1 more
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,Lee Zou +1 more
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.
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Present and Future Perspective on PLK1 Inhibition in Cancer Treatment
Michela Chiappa,Sabrina Petrella,Giovanna Damia,Massimo Broggini,Federica Guffanti,Francesco Ricci +5 more
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.
References
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Journal ArticleDOI
How the Eukaryotic Replisome Achieves Rapid and Efficient DNA Replication.
TL;DR: It is proposed that switching between these DNA polymerases also contributes to leading-strand synthesis under conditions of replicative stress.
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Chk1 promotes replication fork progression by controlling replication initiation
TL;DR: It is suggested that increased replication initiation leads to slow replication forks progression and that Chk1 promotes replication fork progression during normal S phase by controlling replication origin activity.
Journal ArticleDOI
PLK1, A Potential Target for Cancer Therapy.
TL;DR: PLK1’s structural characteristics, its regulatory roles in cell mitosis, PLK1 expression, and its association with survival prognoses of cancer patients in a wide variety of cancer types, PLk1 interaction networks, and PLK 1 inhibitors under investigation are examined.
Journal ArticleDOI
Replication stress interferes with histone recycling and predeposition marking of new histones.
Zuzana Jasencakova,Annette N. D. Scharf,Katrine Ask,Armelle Corpet,Axel Imhof,Geneviève Almouzni,Anja Groth +6 more
TL;DR: This work identifies marks on histones H3-H4 bound to Asf1 and changes induced upon replication stress and shows that replication stress interferes with predeposition marking and histone recycling with potential impact on epigenetic stability.
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The BRCA1-RAP80 complex regulates DNA repair mechanism utilization by restricting end resection.
TL;DR: A model is proposed in which the BRCA1-RAP80 complex limits nuclease accessibility to DSBs, thus preventing excessive end resection and potentially deleterious homology-directed DSB repair mechanisms that can impair genome integrity.
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