ArticleThe Journal of cell biology2003
Bloom syndrome cells undergo p53-dependent apoptosis and delayed assembly of BRCA1 and NBS1 repair complexes at stalled replication forks.
Article in The Journal of cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 99 citations in OpenAlex.
- Mitotic BLM functions are required to maintain genomic stability.Nucleic acids research · 2026Article
- Condensin II interacts with BLM helicase in S phase to maintain genome stability.Communications biology · 2025Article
- Review
- RecQ Helicase Somatic Alterations in Cancer.Frontiers in molecular biosciences · 2022Review
- USP37 regulates DNA damage response through stabilizing and deubiquitinating BLM.Nucleic acids research · 2021Article
- A novel cell-cycle-regulated interaction of the Bloom syndrome helicase BLM with Mcm6 controls replication-linked processes.Nucleic acids research · 2021Article
- Functions of BLM Helicase in Cells: Is It Acting Like a Double-Edged Sword?Frontiers in genetics · 2021Review
- MRN complex-dependent recruitment of ubiquitylated BLM helicase to DSBs negatively regulates DNA repair pathways.Nature communications · 2018Article
- RECQ-like helicases Sgs1 and BLM regulate R-loop-associated genome instability.The Journal of cell biology · 2017Article
- Analysis of alternative lengthening of telomere markers in BRCA1 defective cells.Genes, chromosomes & cancer · 2016Article
- The role of post-translational modifications in fine-tuning BLM helicase function during DNA repair.DNA repair · 2014Review
- Article
- Damaged mitochondria in Fanconi anemia - an isolated event or a general phenomenon?Oncoscience · 2014Article
- Smc5/6-mediated regulation of replication progression contributes to chromosome assembly during mitosis in human cells.Molecular biology of the cell · 2014Article
- p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes.The Journal of cell biology · 2013Article
- On BLM helicase in recombination-mediated telomere maintenance.Molecular biology reports · 2013Article
- BLM SUMOylation regulates ssDNA accumulation at stalled replication forks.Frontiers in genetics · 2013Article
- An N-terminal acidic region of Sgs1 interacts with Rpa70 and recruits Rad53 kinase to stalled forks.The EMBO journal · 2012Article
- RMI1 promotes DNA replication fork progression and recovery from replication fork stress.Molecular and cellular biology · 2012Article
- The DNA repair endonuclease XPG interacts directly and functionally with the WRN helicase defective in Werner syndrome.Cell cycle (Georgetown, Tex.) · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Bloom syndrome (BS) is a hereditary disorder characterized by pre- and postnatal growth retardation, genomic instability, and cancer. BLM, the gene defective in BS, encodes a DNA helicase thought to participate in genomic maintenance. We show that BS human fibroblasts undergo extensive apoptosis after DNA damage specifically when DNA replication forks are stalled. Damage during S, but not G1, caused BLM to rapidly form foci with gammaH2AX at replication forks that develop DNA breaks. These BLM foci recruited BRCA1 and NBS1. Damaged BS cells formed BRCA1/NBS1 foci with markedly delayed kinetics. Helicase-defective BLM showed dominant-negative activity with respect to apoptosis, but not BRCA1/NBS1 recruitment, suggesting catalytic and structural roles for BLM. Strikingly, inactivation of p53 prevented the death of damaged BS cells and delayed recruitment of BRCA1/NBS1. These findings suggest that BLM is an early responder to damaged replication forks. Moreover, p53 eliminates cells that rapidly assemble BRCA1/NBS1 without BLM, suggesting that BLM is essential for timely BRCA1/NBS1 function.
Indexed as
Identifiers
What OpenQuestion holds
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.