ArticleCarcinogenesis2008
Phosphorylation-dependent interactions of BLM and 53BP1 are required for their anti-recombinogenic roles during homologous recombination.
Article in Carcinogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- BLM regulates MALT1-driven NF-κB signalling and is targetable in B-cell malignancies.Cell death & disease · 2026Article
- Genetic modeling of ELP1-associated Sonic hedgehog medulloblastoma identifies MDM2 as a selective therapeutic target.Cancer cell · 2025Article
- Phosphorylated BLM peptide acts as an agonist for DNA damage response.Nucleic acids research · 2025Article
- TFIP11 promotes replication fork reversal to preserve genome stability.Nature communications · 2024Article
- A POLD3/BLM dependent pathway handles DSBs in transcribed chromatin upon excessive RNA:DNA hybrid accumulation.Nature communications · 2022Article
- Functions of BLM Helicase in Cells: Is It Acting Like a Double-Edged Sword?Frontiers in genetics · 2021Review
- Bloom Syndrome Protein Activates AKT and PRAS40 in Prostate Cancer Cells.Oxidative medicine and cellular longevity · 2019Article
- MRN complex-dependent recruitment of ubiquitylated BLM helicase to DSBs negatively regulates DNA repair pathways.Nature communications · 2018Article
- 53BP1 can limit sister-chromatid rupture and rearrangements driven by a distinct ultrafine DNA bridging-breakage process.Nature communications · 2018Article
- BLM's balancing act and the involvement of FANCJ in DNA repair.Cell cycle (Georgetown, Tex.) · 2018Article
- BLM helicase regulates DNA repair by counteracting RAD51 loading at DNA double-strand break sites.The Journal of cell biology · 2017Article
- SLX4 Prevents GEN1-Dependent DSBs During DNA Replication Arrest Under Pathological Conditions in Human Cells.Scientific reports · 2017Article
- Regulation of BLM Nucleolar Localization.Genes · 2016Article
- Article
- Cooperation of Blm and Mus81 in development, fertility, genomic integrity and cancer suppression.Oncogene · 2015Article
- The role of post-translational modifications in fine-tuning BLM helicase function during DNA repair.DNA repair · 2014Review
- DNA damage response: three levels of DNA repair regulation.Cold Spring Harbor perspectives in biology · 2013Review
- Ubiquitin-dependent recruitment of the Bloom syndrome helicase upon replication stress is required to suppress homologous recombination.The EMBO journal · 2013Article
- Chromosome breakage is regulated by the interaction of the BLM helicase and topoisomerase IIalpha.Cancer research · 2011Article
- Time to bloom.Genome integrity · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in bloom helicase protein (BLM) helicase cause Bloom syndrome, characterized by predisposition to almost all forms of cancer. We have demonstrated previously that endogenous BLM, signal transducer 53BP1 and RAD51 are present in a complex during replication stress. Using full-length recombinant proteins, we now provide evidence that these proteins physically interact. BLM interacts with checkpoint kinase (Chk) 1 via the kinetochore-binding domain (KBD). Wild-type (WT) Chk1 phosphorylates 53BP1 in the KBD, both in vitro and in vivo during replication stress. Chk1-mediated phosphorylation of 53BP1 enhances its binding to BLM and is required for the accumulation of 53BP1 at the site of stalled replication. 53BP1, in turn, binds to the N-terminal domain of BLM. Ataxia telangiectasia and Rad3 related (ATR)-mediated phosphorylation of BLM at Thr99 is critical for its interaction and subsequent co-localization with 53BP1. WT BLM enhances the interaction and co-localization between 53BP1 and RAD51 during replication arrest. Interactions between the three proteins have functional consequences. Non-binding or phosphorylation-deficient mutants of BLM and 53BP1 fail to demonstrate the anti-recombinogenic property of the WT counterparts. Consequently, these mutants cause elevation of endogenous RAD51 foci formation. These results provide evidence that the phosphorylation-mediated interactions between BLM, 53BP1 and RAD51 are required for their regulatory roles during homologous recombination.
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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.