ReviewDNA repair2016
Fanconi anemia proteins in telomere maintenance.
Review in DNA repair, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 25 citations in OpenAlex.
- Modified iPOND revealed the role of mutant p53 in promoting helicase function and telomere maintenance.Aging · 2023Article
- p53 in the Molecular Circuitry of Bone Marrow Failure Syndromes.International journal of molecular sciences · 2023Review
- Cytogenetics in Fanconi Anemia: The Importance of Follow-Up and the Search for New Biomarkers of Genomic Instability.International journal of molecular sciences · 2022Review
- Intracranial calcification and psychotic symptoms after irradiation in a patient with Fanconi anemia: A case report.PCN reports : psychiatry and clinical neurosciences · 2022Article
- Genome-wide whole-blood transcriptome profiling across inherited bone marrow failure subtypes.Blood advances · 2021Article
- Beyond DNA repair and chromosome instability-Fanconi anaemia as a cellular senescence-associated syndrome.Cell death and differentiation · 2021Review
- A Mendelian randomization study of telomere length and blood-cell traits.Scientific reports · 2020Article
- Cellular and molecular architecture of hematopoietic stem cells and progenitors in genetic models of bone marrow failure.JCI insight · 2020Article
- Proteomic profiling and bioinformatics analysis identify key regulators during the process from fanconi anemia to acute myeloid leukemia.American journal of translational research · 2020Article
- Fanconi anemia proteins counteract the implementation of the oncogene-induced senescence program.Scientific reports · 2019Article
- The FANCM-BLM-TOP3A-RMI complex suppresses alternative lengthening of telomeres (ALT).Nature communications · 2019Article
- Genetic analyses of aplastic anemia and idiopathic pulmonary fibrosis patients with short telomeres, possible implication of DNA-repair genes.Orphanet journal of rare diseases · 2019Article
- Telomere length and telomerase activity during folliculogenesis in mammals.The Journal of reproduction and development · 2018Review
- Multiplexed CRISPR/Cas9-mediated knockout of 19 Fanconi anemia pathway genes in zebrafish revealed their roles in growth, sexual development and fertility.PLoS genetics · 2018Article
- Review
- FANCM, BRCA1, and BLM cooperatively resolve the replication stress at the ALT telomeres.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- SNM1B/Apollo in the DNA damage response and telomere maintenance.Oncotarget · 2017Review
- Mgm101: A double-duty Rad52-like protein.Cell cycle (Georgetown, Tex.) · 2016Article
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
Mammalian chromosome ends are protected by nucleoprotein structures called telomeres. Telomeres ensure genome stability by preventing chromosome termini from being recognized as DNA damage. Telomere length homeostasis is inevitable for telomere maintenance because critical shortening or over-lengthening of telomeres may lead to DNA damage response or delay in DNA replication, and hence genome instability. Due to their repetitive DNA sequence, unique architecture, bound shelterin proteins, and high propensity to form alternate/secondary DNA structures, telomeres are like common fragile sites and pose an inherent challenge to the progression of DNA replication, repair, and recombination apparatus. It is conceivable that longer the telomeres are, greater is the severity of such challenges. Recent studies have linked excessively long telomeres with increased tumorigenesis. Here we discuss telomere abnormalities in a rare recessive chromosomal instability disorder called Fanconi Anemia and the role of the Fanconi Anemia pathway in telomere biology. Reports suggest that Fanconi Anemia proteins play a role in maintaining long telomeres, including processing telomeric joint molecule intermediates. We speculate that ablation of the Fanconi Anemia pathway would lead to inadequate aberrant structural barrier resolution at excessively long telomeres, thereby causing replicative burden on the cell.
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.