ArticleProceedings of the National Academy of Sciences of the United States of America2002
Ku86 is essential in human somatic cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 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
80 citing papers in PubMed, 203 citations in OpenAlex.
- Uncovering genetic interactions in the DNA repair network in response to endogenous damage and ionizing radiation.Cell reports · 2026Article
- PARP1 and PARP2 are dispensable for DNA repair by microhomology-mediated end-joining at double-ended DSBs.Nucleic acids research · 2026Article
- Primate-specific adaptation of Ku protects transcriptomic integrity by suppressing Alu-mediated alternative splicing.bioRxiv : the preprint server for biology · 2025Article
- Ku limits aberrant mRNA splicing promoted by intronic antisense Alu elements.bioRxiv : the preprint server for biology · 2025Article
- The nuclear phosphoinositide-p53 signalosome in the regulation of cell motility.Protein & cell · 2025Review
- Article
- Targeting DNA damage sensors for cancer therapy.DNA repair · 2025Review
- Conversion of Ku80 K568 crotonylation to SUMOylation facilitates DNA non-homologous end joining and cancer radioresistance.Signal transduction and targeted therapy · 2025Article
- Growth hormone and radiation therapy: friend, foe, or both?Endocrine-related cancer · 2024Review
- Noncanonical functions of Ku may underlie essentiality in human cells.Scientific reports · 2023Article
- The APE2 nuclease is essential for DNA double-strand break repair by microhomology-mediated end joining.Molecular cell · 2023Article
- Ku-DNA binding inhibitors modulate the DNA damage response in response to DNA double-strand breaks.NAR cancer · 2023Article
- Doxycycline Attenuated Ethanol-Induced Inflammaging in Endothelial Cells: Implications in Alcohol-Mediated Vascular Diseases.Antioxidants (Basel, Switzerland) · 2022Article
- Article
- DNA End Joining: G0-ing to the Core.Biomolecules · 2021Review
- Review
- The Ku complex: recent advances and emerging roles outside of non-homologous end-joining.Cellular and molecular life sciences : CMLS · 2021Review
- Improved Genome Editing through Inhibition of FANCM and Members of the BTR Dissolvase Complex.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Deficiency of Ku Induces Host Cell Exploitation in Human Cancer Cells.Frontiers in cell and developmental biology · 2021Article
- Suppression of non-homologous end joining does not rescue DNA repair defects in Fanconi anemia patient cells.Cell cycle (Georgetown, Tex.) · 2020Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Ku86 plays a key role in nonhomologous end joining in mammals. Functional inactivation in rodents of either Ku86 or Ku70, which form the heterodimeric DNA end-binding subunit of the DNA-dependent protein kinase complex, is nevertheless compatible with viability. In contrast, no human patient has been described with mutations in either Ku86 or Ku70. This has led to the hypotheses that either these genes are performing an additional essential role(s) and/or redundant pathways exist that mask the phenotypic expression of these genes when they are mutated in humans. To address this issue, we describe here the construction of human somatic cell lines containing a targeted disruption of the Ku86 locus. Human HCT116 colon cancer cells heterozygous for Ku86 were haploinsufficient with an increase in polyploid cells, a reduction in cell proliferation, elevated p53 levels, and a slight hypersensitivity to ionizing radiation. Functional inactivation of the second Ku86 allele resulted in cells with a drastically reduced doubling time. These cells were capable of undergoing only a limited number of cell divisions, after which they underwent apoptosis. These experiments demonstrate that the Ku86 locus is essential in human somatic tissue culture cells.
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.