ArticleNucleic acids research2023
LncRNA HOTAIRM1 functions in DNA double-strand break repair via its association with DNA repair and mRNA surveillance factors.
Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- LINC00839 transcriptionally activated by ELK1 represses ferroptosis in nasopharyngeal carcinoma by regulating UPF1/RCHY1/DJ-1 axis.NPJ precision oncology · 2026Article
- Multiomic single-cell perturbation screens reveal critical lncRNA regulators of senescence.Nature aging · 2026Article
- Long Noncoding RNA function prediction via multiview cross-contrastive learning combined with multiscale semantic adaptive optimization.Briefings in bioinformatics · 2025Article
- Article
- Long noncoding RNA AK144717 exacerbates pathological cardiac hypertrophy through modulating the cellular distribution of HMGB1 and subsequent DNA damage response.Cellular and molecular life sciences : CMLS · 2024Article
- LncRNA HOTAIRM1 promotes radioresistance in nasopharyngeal carcinoma by modulating FTO acetylation-dependent alternative splicing of CD44.Neoplasia (New York, N.Y.) · 2024Article
- Deciphering shared attributes of plant long non-coding RNAs through a comparative computational approach.Scientific reports · 2023Article
- Co-phase separation of Y14 and RNA in vitro and its implication for DNA repair.RNA (New York, N.Y.) · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The eukaryotic exon junction complex component Y14 participates in double-strand break (DSB) repair via its RNA-dependent interaction with the non-homologous end-joining (NHEJ) complex. Using immunoprecipitation-RNA-seq, we identified a set of Y14-associated long non-coding RNAs (lncRNAs). The lncRNA HOTAIRM1 serves as a strong candidate that mediates the interaction between Y14 and the NHEJ complex. HOTAIRM1 localized to near ultraviolet laser-induced DNA damage sites. Depletion of HOTAIRM1 delayed the recruitment of DNA damage response and repair factors to DNA lesions and compromised the efficiency of NHEJ-mediated DSB repair. Identification of the HOTAIRM1 interactome revealed a large set of RNA processing factors including mRNA surveillance factors. The surveillance factors Upf1 and SMG6 localized to DNA damage sites in a HOTAIRM1-dependent manner. Depletion of Upf1 or SMG6 increased the level of DSB-induced non-coding transcripts at damaged sites, indicating a pivotal role for Upf1/SMG6-mediated RNA degradation in DNA repair. We conclude that HOTAIRM1 serves as an assembly scaffold for both DNA repair and mRNA surveillance factors that act in concert to repair DSBs.
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