ArticleNucleic acids research2017
Human MLH1 suppresses the insertion of telomeric sequences at intra-chromosomal sites in telomerase-expressing cells.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Molecular and functional characterization of telomeric repeat-containing RNAs in Chinese hamster ovary cells.Nucleic acids research · 2026Article
- The marsupial imprinted gene MLH1 has retrocopies in three marsupial families.Epigenetics & chromatin · 2026Article
- The ubiquitin ligase UBR4 and the deubiquitylase USP5 modulate the stability of DNA mismatch repair protein MLH1.The Journal of biological chemistry · 2024Article
- ATR blocks telomerase from converting DNA breaks into telomeres.Science (New York, N.Y.) · 2024Article
- Telomerase subunit Est2 marks internal sites that are prone to accumulate DNA damage.BMC biology · 2021Article
- SERPINH1 is a Potential Prognostic Biomarker and Correlated With Immune Infiltration: A Pan-Cancer Analysis.Frontiers in genetics · 2021Article
- Full length RTEL1 is required for the elongation of the single-stranded telomeric overhang by telomerase.Nucleic acids research · 2020Article
- Genomic footprints of activated telomere maintenance mechanisms in cancer.Nature communications · 2020Article
- Werner Syndrome Helicase Is Required for the Survival of Cancer Cells with Microsatellite Instability.iScience · 2019Article
- Review
- The MLH1 ATPase domain is needed for suppressing aberrant formation of interstitial telomeric sequences.DNA repair · 2018Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Aberrant formation of interstitial telomeric sequences (ITSs) promotes genome instabilities. However, it is unclear how aberrant ITS formation is suppressed in human cells. Here, we report that MLH1, a key protein involved in mismatch repair (MMR), suppresses telomeric sequence insertion (TSI) at intra-chromosomal regions. The frequency of TSI can be elevated by double-strand break (DSB) inducer and abolished by ATM/ATR inhibition. Suppression of TSI requires MLH1 recruitment to DSBs, indicating that MLH1's role in DSB response/repair is important for suppressing TSI. Moreover, TSI requires telomerase activity but is independent of the functional status of p53 and Rb. Lastly, we show that TSI is associated with chromosome instabilities including chromosome loss, micronuclei formation and chromosome breakage that are further elevated by replication stress. Our studies uncover a novel link between MLH1, telomerase, telomere and genome stability.
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