ArticleGenes & development2019
RAD52 and SLX4 act nonepistatically to ensure telomere stability during alternative telomere lengthening.
Article in Genes & development, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
What it found
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Who cites it
87 citing papers in PubMed, 109 citations in OpenAlex.
- Beyond End Protection: Shelterin, POT1 Dysfunction, and Telomere Replication Stress in Cancer.Biomolecules · 2026Review
- Telomere-to-telomere genome assembly of Microsporidia sp. MB, a microsporidian symbiont of Anopheles coluzzii isolated from Burkina Faso.BMC genomics · 2026Article
- Mechanism and potential therapeutic strategies of genetic abnormalities involved in deoxyribonucleic acid double-strand breaks leading to the development of human non-obstructive azoospermia.Reproductive biology and endocrinology : RB&E · 2026Review
- NPM1 phosphorylation-mediated telomere maintenance via stabilization of POLD3 in ALT-positive osteosarcoma: unraveling mechanisms and therapeutic opportunities.Theranostics · 2026Article
- The alternative lengthening of telomeres pathway through a DNA repair lens: mechanism and therapeutic opportunities.NAR cancer · 2025Review
- Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025Review
- Atypical R-loops in cancer: decoding molecular chaos for therapeutic gain.Journal of translational medicine · 2025Review
- Identification of telomere maintenance related biomarkers and regulatory mechanisms in chronic obstructive pulmonary disease by machine learning algorithm.Scientific reports · 2025Article
- TRIM24 directs replicative stress responses to maintain ALT telomeres via chromatin signaling.Molecular cell · 2025Article
- Monomers and short oligomers of human RAD52 promote single-strand annealing.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Biomolecular Condensates in Telomere Maintenance of ALT Cancer Cells.Journal of molecular biology · 2025Review
- TERRA and the alternative lengthening of telomeres: a dangerous affair.FEBS letters · 2025Review
- RAD52 and ERCC6L/PICH have a compensatory relationship for genome stability in mitosis.PLoS genetics · 2024Article
- LAP2α orchestrates alternative lengthening of telomeres suppression through telomeric heterochromatin regulation with HDAC1: unveiling a potential therapeutic target.Cell death & disease · 2024Article
- SUMO promotes DNA repair protein collaboration to support alternative telomere lengthening in the absence of PML.Genes & development · 2024Article
- Mechanisms of telomere maintenance and associated therapeutic vulnerabilities in malignant gliomas.Neuro-oncology · 2024Review
- BLM helicase unwinds lagging strand substrates to assemble the ALT telomere damage response.Molecular cell · 2024Article
- Article
- PARP2 promotes Break Induced Replication-mediated telomere fragility in response to replication stress.Nature communications · 2024Article
- Targeting ATR in patients with cancer.Nature reviews. Clinical oncology · 2024Review
27 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Approximately 15% of cancers use homologous recombination for alternative lengthening of telomeres (ALT). How the initiating genomic lesions invoke homology-directed telomere synthesis remains enigmatic. Here, we show that distinct dependencies exist for telomere synthesis in response to replication stress or DNA double-strand breaks (DSBs). RAD52 deficiency reduced spontaneous telomeric DNA synthesis and replication stress-associated recombination in G2, concomitant with telomere shortening and damage. However, viability and proliferation remained unaffected, suggesting that alternative telomere recombination mechanisms compensate in the absence of RAD52. In agreement, RAD52 was dispensable for DSB-induced telomere synthesis. Moreover, a targeted CRISPR screen revealed that loss of the structure-specific endonuclease scaffold SLX4 reduced the proliferation of RAD52-null ALT cells. While SLX4 was dispensable for RAD52-mediated ALT telomere synthesis in G2, combined SLX4 and RAD52 loss resulted in elevated telomere loss, unresolved telomere recombination intermediates, and mitotic infidelity. These findings establish that RAD52 and SLX4 mediate distinct postreplicative DNA repair processes that maintain ALT telomere stability and cancer cell viability.
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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.