ArticleMolecular cancer research : MCR2010
Chk1-dependent constitutive phosphorylation of BLM helicase at serine 646 decreases after DNA damage.
Article in Molecular cancer research : MCR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 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
- Condensin II interacts with BLM helicase in S phase to maintain genome stability.Communications biology · 2025Article
- Phosphorylated BLM peptide acts as an agonist for DNA damage response.Nucleic acids research · 2025Article
- The CDK1-TOPBP1-PLK1 axis regulates the Bloom's syndrome helicase BLM to suppress crossover recombination in somatic cells.Science advances · 2022Article
- USP37 regulates DNA damage response through stabilizing and deubiquitinating BLM.Nucleic acids research · 2021Article
- 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
- DNA damage kinase signaling: checkpoint and repair at 30 years.The EMBO journal · 2019Review
- A tri-serine cluster within the topoisomerase IIα-interaction domain of the BLM helicase is required for regulating chromosome breakage in human cells.Human molecular genetics · 2018Article
- MRN complex-dependent recruitment of ubiquitylated BLM helicase to DSBs negatively regulates DNA repair pathways.Nature communications · 2018Article
- Regulation of BLM Nucleolar Localization.Genes · 2016Article
- A Network of Conserved Synthetic Lethal Interactions for Exploration of Precision Cancer Therapy.Molecular cell · 2016Article
- Article
- Chemogenetic profiling identifies RAD17 as synthetically lethal with checkpoint kinase inhibition.Oncotarget · 2015Article
- The role of post-translational modifications in fine-tuning BLM helicase function during DNA repair.DNA repair · 2014Review
- Roles of Chk1 in cell biology and cancer therapy.International journal of cancer · 2014Review
- Article
- Ubiquitin-dependent recruitment of the Bloom syndrome helicase upon replication stress is required to suppress homologous recombination.The EMBO journal · 2013Article
- Time to bloom.Genome integrity · 2010Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
BLM helicase, the protein mutated in Bloom syndrome, is involved in signal transduction cascades after DNA damage. BLM is phosphorylated on multiple residues by different kinases either after stress induction or during mitosis. Here, we have provided evidence that both Chk1 and Chk2 phosphorylated the NH(2)-terminal 660 amino acids of BLM. An internal region within the DExH motif of BLM negatively regulated the Chk1/Chk2-dependent NH(2)-terminal phosphorylation event. Using in silico analysis involving the Chk1 structure and its known substrate specificity, we predicted that Chk1 should preferentially phosphorylate BLM on serine 646 (Ser(646)). The prediction was validated in vitro by phosphopeptide analysis on BLM mutants and in vivo by usage of a newly generated phosphospecific polyclonal antibody. We showed that the phosphorylation at Ser(646) on BLM was constitutive and decreased rapidly after exposure to DNA damage. This resulted in the diminished interaction of BLM with nucleolin and PML isoforms, and consequently decreased BLM accumulation in the nucleolus and PML nuclear bodies. Instead, BLM relocalized to the sites of DNA damage and bound with the damage sensor protein, Nbs1. Mutant analysis confirmed that the binding to nucleolin and PML isoforms required Ser(646) phosphorylation. These results indicated that Chk1-mediated phosphorylation on BLM at Ser(646) might be a determinant for regulating subnuclear localization and could act as a marker for the activation status of BLM in response to DNA damage.
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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.