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Simon Bekker-Jensen

Researcher at University of Copenhagen

Publications -  83
Citations -  12184

Simon Bekker-Jensen is an academic researcher from University of Copenhagen. The author has contributed to research in topics: Chromatin & DNA repair. The author has an hindex of 44, co-authored 68 publications receiving 10818 citations. Previous affiliations of Simon Bekker-Jensen include Foundation Center & University of Copenhagen Faculty of Health Sciences.

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RNF8 Ubiquitylates Histones at DNA Double-Strand Breaks and Promotes Assembly of Repair Proteins

TL;DR: It is suggested that MDC1-mediated and RNF8-executed histone ubiquitylation protects genome integrity by licensing the DSB-flanking chromatin to concentrate repair factors near the DNA lesions.
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RNF168 Binds and Amplifies Ubiquitin Conjugates on Damaged Chromosomes to Allow Accumulation of Repair Proteins

TL;DR: Evidence is provided that, while RNF8 is necessary to trigger the DSB-associated ubiquitylation, it is not sufficient to sustain conjugated ubiquitin in this compartment, which defines a new pathway involving sequential ubiquitylations on damaged chromosomes and uncovers a functional cooperation between E3 ligases in genome maintenance.
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Chromatin relaxation in response to DNA double-strand breaks is modulated by a novel ATM- and KAP-1 dependent pathway

TL;DR: It is shown that DSB formation is followed by ATM-dependent chromatin relaxation, which suggests that chromatin Relaxation is a fundamental pathway in the DNA-damage response and identifies its primary mediators.
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ATR Prohibits Replication Catastrophe by Preventing Global Exhaustion of RPA

TL;DR: ATR-mediated suppression of dormant origins shields active forks against irreversible breakage via preventing exhaustion of nuclear RPA, elucidates how replicating genomes avoid destabilizing DNA damage and provides a molecular rationale for their hypersensitivity to ATR inhibitors.
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Spatial organization of the mammalian genome surveillance machinery in response to DNA strand breaks

TL;DR: It is proposed that subclassification of DSB regulators according to their residence sites provides a useful framework for understanding their involvement in diverse processes of genome surveillance.