ArticleOncotarget2016
BLM promotes the activation of Fanconi Anemia signaling pathway.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Review
- Replication stress responses in human lymphocytes change sex-specifically during aging.Nucleic acids research · 2025Article
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- Review
- Dynamic switching of crotonylation to ubiquitination of H2A at lysine 119 attenuates transcription-replication conflicts caused by replication stress.Nucleic acids research · 2022Article
- Single-cell transcription profiles in Bloom syndrome patients link BLM deficiency with altered condensin complex expression signatures.Human molecular genetics · 2022Article
- The BLM helicase is a new therapeutic target in multiple myeloma involved in replication stress survival and drug resistance.Frontiers in immunology · 2022Article
- Regulation of interference-sensitive crossover distribution ensures crossover assurance inProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- An Arabidopsis FANCJ helicase homologue is required for DNA crosslink repair and rDNA repeat stability.PLoS genetics · 2019Article
- A new look at molecular biology of breast cancer.Cancer biology & therapy · 2019Review
- Multifaceted Fanconi Anemia Signaling.Trends in genetics : TIG · 2018Review
- BLM's balancing act and the involvement of FANCJ in DNA repair.Cell cycle (Georgetown, Tex.) · 2018Article
- RECQ-like helicases Sgs1 and BLM regulate R-loop-associated genome instability.The Journal of cell biology · 2017Article
- Fanconi Anemia Signaling and Cancer.Trends in cancer · 2017Review
- FANCD2 and DNA Damage.International journal of molecular sciences · 2017Review
- Osteosarcoma: Molecular Pathogenesis and iPSC Modeling.Trends in molecular medicine · 2017Review
- Involvement of FANCD2 in Energy Metabolism via ATP5α.Scientific reports · 2017Article
- Maintenance of genome stability by Fanconi anemia proteins.Cell & bioscience · 2017Review
- Fanconi Anemia Group D2 Protein Participates in Replication Origin Firing.Chemotherapy · 2016Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
Mutations in the human RecQ helicase, BLM, causes Bloom Syndrome, which is a rare autosomal recessive disorder and characterized by genomic instability and an increased risk of cancer. Fanconi Anemia (FA), resulting from mutations in any of the 19 known FA genes and those yet to be known, is also characterized by chromosomal instability and a high incidence of cancer. BLM helicase and FA proteins, therefore, may work in a common tumor-suppressor signaling pathway. To date, it remains largely unclear as to how BLM and FA proteins work concurrently in the maintenance of genome stability. Here we report that BLM is involved in the early activation of FA group D2 protein (FANCD2). We found that FANCD2 activation is substantially delayed and attenuated in crosslinking agent-treated cells harboring deficient Blm compared to similarly treated control cells with sufficient BLM. We also identified that the domain VI of BLM plays an essential role in promoting FANCD2 activation in cells treated with DNA crosslinking agents, especially ultraviolet B. The similar biological effects performed by ΔVI-BLM and inactivated FANCD2 further confirm the relationship between BLM and FANCD2. Mutations within the domain VI of BLM detected in human cancer samples demonstrate the functional importance of this domain, suggesting human tumorigenicity resulting from mtBLM may be at least partly attributed to mitigated FANCD2 activation. Collectively, our data show a previously unknown regulatory liaison in advancing our understanding of how the cancer susceptibility gene products act in concert to maintain 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.