ArticleCell death and differentiation2020
LRIK interacts with the Ku70-Ku80 heterodimer enhancing the efficiency of NHEJ repair.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- LncRNAs: key regulators and molecular mechanisms in lung cancer radiosensitivity.Open medicine (Warsaw, Poland) · 2026Review
- Airborne PMInternational journal of molecular sciences · 2025Article
- LncRNA-Protein Interactions: A Key to Deciphering LncRNA Mechanisms.Biomolecules · 2025Review
- Long non-coding RNANon-coding RNA research · 2024Article
- CircCDYL2 bolsters radiotherapy resistance in nasopharyngeal carcinoma by promoting RAD51 translation initiation for enhanced homologous recombination repair.Journal of experimental & clinical cancer research : CR · 2024Article
- ATR-binding lncRNA ScaRNA2 promotes cancer resistance through facilitating efficient DNA end resection during homologous recombination repair.Journal of experimental & clinical cancer research : CR · 2023Article
- The N-Myc-responsive lncRNA MILIP promotes DNA double-strand break repair through non-homologous end joining.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- CCAR2 functions downstream of the Shieldin complex to promote double-strand break end-joining.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Long non-coding RNAs affecting cell metabolism in cancer.Biology direct · 2022Review
- Long non‑coding RNAs interact with RNA‑binding proteins to regulate genomic instability in cancer cells (Review).Oncology reports · 2022Review
- Review
- Article
- Long Noncoding RNA NIHCOLE Promotes Ligation Efficiency of DNA Double-Strand Breaks in Hepatocellular Carcinoma.Cancer research · 2021Article
- Home and Away: The Role of Non-Coding RNA in Intracellular and Intercellular DNA Damage Response.Genes · 2021Review
- The evolving complexity of DNA damage foci: RNA, condensates and chromatin in DNA double-strand break repair.DNA repair · 2021Review
- VAV2 is required for DNA repair and implicated in cancer radiotherapy resistance.Signal transduction and targeted therapy · 2021Article
- DCTPP1, an Oncogene Regulated by miR-378a-3p, Promotes Proliferation of Breast Cancer via DNA Repair Signaling Pathway.Frontiers in oncology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite recent advances in our understanding of the function of long noncoding RNAs (lncRNAs), their roles and functions in DNA repair pathways remain poorly understood. By screening a panel of uncharacterized lncRNAs to identify those whose transcription is induced by double-strand breaks (DSBs), we identified a novel lncRNA referred to as LRIK that interacts with Ku, which enhances the ability of the Ku heterodimer to detect the presence of DSBs. Here, we show that depletion of LRIK generates significantly enhanced sensitivity to DSB-inducing agents and reduced DSB repair efficiency. In response to DSBs, LRIK enhances the recruitment of repair factors at DSB sites and facilitates γH2AX signaling. Our results demonstrate that LRIK is necessary for efficient repairing DSBs via nonhomologous end-joining pathway.
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.