ArticleThe EMBO journal2013
Ubiquitin-dependent recruitment of the Bloom syndrome helicase upon replication stress is required to suppress homologous recombination.
Article in The EMBO journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- K63-linked ubiquitylation of RMI1 by RNF8 is essential to its recruitment to stalled forks.Cellular and molecular life sciences : CMLS · 2026Article
- Mitotic BLM functions are required to maintain genomic stability.Nucleic acids research · 2026Article
- The role of HECT-type E3 ubiquitin ligases in DNA damage response and repair.Cell death discovery · 2025Review
- Phosphorylated BLM peptide acts as an agonist for DNA damage response.Nucleic acids research · 2025Article
- PCNA-binding activity separates RNF168 functions in DNA replication and DNA double-stranded break signaling.Nucleic acids research · 2024Article
- CRISPR/Cas9-mediated knockout of the ubiquitin variant UbKEKS reveals a role in regulating nucleolar structures and composition.Biology open · 2023Article
- Emerging Roles of Non-proteolytic Ubiquitination in Tumorigenesis.Frontiers in cell and developmental biology · 2022Review
- USP37 regulates DNA damage response through stabilizing and deubiquitinating BLM.Nucleic acids research · 2021Article
- RNF168 regulates R-loop resolution and genomic stability in BRCA1/2-deficient tumors.The Journal of clinical investigation · 2021Article
- MRN complex is an essential effector of DNA damage repair.Journal of Zhejiang University. Science. B · 2021Review
- HERC2 inactivation abrogates nucleolar localization of RecQ helicases BLM and WRN.Scientific reports · 2021Article
- Functions of BLM Helicase in Cells: Is It Acting Like a Double-Edged Sword?Frontiers in genetics · 2021Review
- FANCJ compensates for RAP80 deficiency and suppresses genomic instability induced by interstrand cross-links.Nucleic acids research · 2020Article
- The Promyelocytic Leukemia Protein facilitates human herpesvirus 6B chromosomal integration, immediate-early 1 protein multiSUMOylation and its localization at telomeres.PLoS pathogens · 2020Article
- Doxorubicin-induced DNA Damage Causes Extensive Ubiquitination of Ribosomal Proteins Associated with a Decrease in Protein Translation.Molecular & cellular proteomics : MCP · 2018Article
- Lesion Bypass and the Reactivation of Stalled Replication Forks.Annual review of biochemistry · 2018Review
- 53BP1 Mediates ATR-Chk1 Signaling and Protects Replication Forks under Conditions of Replication Stress.Molecular and cellular biology · 2018Article
- MRN complex-dependent recruitment of ubiquitylated BLM helicase to DSBs negatively regulates DNA repair pathways.Nature communications · 2018Article
- Ultrastructural and Molecular Analyses Reveal Enhanced Nucleolar Activity inFrontiers in plant science · 2018Article
- Crosstalk between the nucleolus and the DNA damage response.Molecular bioSystems · 2017Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Limiting the levels of homologous recombination (HR) that occur at sites of DNA damage is a major role of BLM helicase. However, very little is known about the mechanisms dictating its relocalization to these sites. Here, we demonstrate that the ubiquitin/SUMO-dependent DNA damage response (UbS-DDR), controlled by the E3 ligases RNF8/RNF168, triggers BLM recruitment to sites of replication fork stalling via ubiquitylation in the N-terminal region of BLM and subsequent BLM binding to the ubiquitin-interacting motifs of RAP80. Furthermore, we show that this mechanism of BLM relocalization is essential for BLM's ability to suppress excessive/uncontrolled HR at stalled replication forks. Unexpectedly, we also uncovered a requirement for RNF8-dependent ubiquitylation of BLM and PML for maintaining the integrity of PML-associated nuclear bodies and as a consequence the localization of BLM to these structures. Lastly, we identified a novel role for RAP80 in preventing proteasomal degradation of BLM in unstressed cells. Taken together, these data highlight an important biochemical link between the UbS-DDR and BLM-dependent pathways involved in maintaining genome stability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.