ArticleTrends in genetics : TIG2012
Fanconi anemia and Bloom's syndrome crosstalk through FANCJ-BLM helicase interaction.
Article in Trends in genetics : TIG, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
39 citing papers in PubMed, 57 citations in OpenAlex.
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- BLM and FANCJ role in the response to G-quadruplex-dependent telomeric replicative stress.Communications biology · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome Protein.International journal of molecular sciences · 2024Review
- The DNA helicase FANCJ (BRIP1) functions in double strand break repair processing, but not crossover formation during prophase I of meiosis in male mice.PLoS genetics · 2024Article
- The DNA helicase FANCJ (BRIP1) functions in Double Strand Break repair processing, but not crossover formation during Prophase I of meiosis in male mice.bioRxiv : the preprint server for biology · 2023Article
- G-Quadruplex-Binding Proteins: Promising Targets for Drug Design.Biomolecules · 2022Review
- The BLM helicase is a new therapeutic target in multiple myeloma involved in replication stress survival and drug resistance.Frontiers in immunology · 2022Article
- Recent Advances in the Development of Non-PIKKs Targeting Small Molecule Inhibitors of DNA Double-Strand Break Repair.Frontiers in oncology · 2022Review
- Comprehensive Mutational Analysis of the BRCA1-Associated DNA Helicase and Tumor-Suppressor FANCJ/BACH1/BRIP1.Molecular cancer research : MCR · 2021Article
- Article
- Distinct roles of BRCA2 in replication fork protection in response to hydroxyurea and DNA interstrand cross-links.Genes & development · 2020Article
- Inherited Variants inCancers · 2019Article
- The MCM8/9 complex: A recent recruit to the roster of helicases involved in genome maintenance.DNA repair · 2019Review
- 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
- Systematic analysis of DNA crosslink repair pathways during development and aging in Caenorhabditis elegans.Nucleic acids research · 2017Article
- Bloom's syndrome: Why not premature aging?: A comparison of the BLM and WRN helicases.Ageing research reviews · 2017Review
- Cellular response to DNA interstrand crosslinks: the Fanconi anemia pathway.Cellular and molecular life sciences : CMLS · 2016Review
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 2 institutions in 1 country.
Funding
Abstract
Fanconi anemia (FA) and Bloom's syndrome (BS) are rare hereditary chromosomal instability disorders. FA displays bone marrow failure, acute myeloid leukemia, and head and neck cancers, whereas BS is characterized by growth retardation, immunodeficiency, and a wide spectrum of cancers. The BLM gene mutated in BS encodes a DNA helicase that functions in a protein complex to suppress sister-chromatid exchange. Of the 15 FA genetic complementation groups implicated in interstrand crosslink repair, FANCJ encodes a DNA helicase involved in recombinational repair and replication stress response. Based on evidence that BLM and FANCJ interact we suggest that crosstalk between BLM and FA pathways is more complex than previously thought. We propose testable models for how FANCJ and BLM coordinate to help cells deal with stalled replication forks or double-strand breaks (DSB). Understanding how BLM and FANCJ cooperate will help to elucidate an important pathway for maintaining genomic stability.
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.