Evidence map›Paper›PMID 39265577›Full record

ArticleCell2024

TEX264 drives selective autophagy of DNA lesions to promote DNA repair and cell survival.

Pauline Lascaux, Gwendoline Hoslett, Sara Tribble, Camilla Trugenberger, Ivan Antičević, Cecile Otten, Ignacio Torrecilla, Stelios Koukouravas, Yichen Zhao, Hongbin Yang and 19 more

Abstract read
PubMed Publisher
In one paragraph

Article in Cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Autophagy modulation in cancer.Nature reviews. Drug discovery · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Food science & nutrition · 2026
    Article
  14. Review
  15. Article
  16. ER membrane receptors engage core autophagy machinery to initiate ER-phagy.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  17. Article
  18. Visualizing DNA repair factor recruitment at sites of transcription in single cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2026
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

29 authors.

Pauline LascauxThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Gwendoline HoslettThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Sara TribbleThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Camilla TrugenbergerThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Ivan AntičevićDNA Damage Group, Laboratory for Molecular Ecotoxicology, Department for Marine and Environmental Research, Institute Ruđer Bošković, 10000 Zagreb, Croatia.
Cecile OttenDNA Damage Group, Laboratory for Molecular Ecotoxicology, Department for Marine and Environmental Research, Institute Ruđer Bošković, 10000 Zagreb, Croatia.
Ignacio TorrecillaThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Stelios KoukouravasThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Yichen ZhaoThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Hongbin YangThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Ftoon AljarbouThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Annamaria RuggianoThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Wei SongThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Cristiano PeronThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Giulio DeangeliDepartment of Clinical Neurosciences, University of Cambridge, Cambridge CB2 2PY, UK.
Enric DomingoDepartment of Oncology, Medical Sciences Division, Old Road Campus Research Building, University of Oxford, Oxford OX3 7DQ, UK.
James BancroftCentre for Human Genetics, Nuffield Department of Medicine (NDM), University of Oxford, Oxford OX3 7BN, UK.
Loïc CarriqueDivision of Structural Biology, Centre for Human Genetics, Nuffield Department of Medicine (NDM), University of Oxford, Oxford OX3 7BN, UK.
Errin JohnsonDunn School Bioimaging Facility, Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.
Iolanda VendrellTarget Discovery Institute, Nuffield Department of Medicine (NDM), University of Oxford, Oxford OX3 7FZ, UK; Chinese Academy for Medical Sciences Oxford Institute, Nuffield Department of Medicine (NDM), University of Oxford, Oxford OX3 7FZ, UK.
Roman FischerTarget Discovery Institute, Nuffield Department of Medicine (NDM), University of Oxford, Oxford OX3 7FZ, UK; Chinese Academy for Medical Sciences Oxford Institute, Nuffield Department of Medicine (NDM), University of Oxford, Oxford OX3 7FZ, UK.
Alvin Wei Tian NgLee Kong Chian School of Medicine (LKCMedicine), Nanyang Technological University, Singapore 636921, Singapore.
Joanne NgeowLee Kong Chian School of Medicine (LKCMedicine), Nanyang Technological University, Singapore 636921, Singapore; Cancer Genetics Service, Division of Medical Oncology, National Cancer Centre Singapore, Singapore 169610, Singapore.
Vincenzo D'AngiolellaThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK; Edinburgh Cancer Research, CRUK Scotland Centre, Institute of Genetics and Cancer, University of Edinburgh, EH4 2XU Edinburgh, UK.
Nuno RaimundoPenn State College of Medicine, Department of Cellular and Molecular Physiology, Hershey, PA 17033, USA; Multidisciplinary Institute for Aging, Center for Innovation in Biomedicine and Biotechnology, University of Coimbra, Coimbra 3000-370, Portugal.
Tim MaughanInstitute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool L69 7BE, UK.
Marta PopovićDNA Damage Group, Laboratory for Molecular Ecotoxicology, Department for Marine and Environmental Research, Institute Ruđer Bošković, 10000 Zagreb, Croatia.
Ira MiloševićCentre for Human Genetics, Nuffield Department of Medicine (NDM), University of Oxford, Oxford OX3 7BN, UK; Multidisciplinary Institute for Aging, Center for Innovation in Biomedicine and Biotechnology, University of Coimbra, Coimbra 3000-370, Portugal.
Kristijan RamadanThe MRC Weatherall Institute of Molecular Medicine, Department of Oncology, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK; Lee Kong Chian School of Medicine (LKCMedicine), Nanyang Technological University, Singapore 636921, Singapore. Electronic address: kristijan.ramadan@ntu.edu.sg.

Funding

Medical Research Council MR/X006409/1
6 · The paper itself

Abstract

DNA repair and autophagy are distinct biological processes vital for cell survival. Although autophagy helps maintain genome stability, there is no evidence of its direct role in the repair of DNA lesions. We discovered that lysosomes process topoisomerase 1 cleavage complexes (TOP1cc) DNA lesions in vertebrates. Selective degradation of TOP1cc by autophagy directs DNA damage repair and cell survival at clinically relevant doses of topoisomerase 1 inhibitors. TOP1cc are exported from the nucleus to lysosomes through a transient alteration of the nuclear envelope and independent of the proteasome. Mechanistically, the autophagy receptor TEX264 acts as a TOP1cc sensor at DNA replication forks, triggering TOP1cc processing by the p97 ATPase and mediating the delivery of TOP1cc to lysosomes in an MRE11-nuclease- and ATR-kinase-dependent manner. We found an evolutionarily conserved role for selective autophagy in DNA repair that enables cell survival, protects genome stability, and is clinically relevant for colorectal cancer patients.

Indexed as

AutophagyCell SurvivalDNA DamageDNA RepairDNA Topoisomerases, Type ILysosomesMembrane ProteinsAnimalsAtaxia Telangiectasia Mutated ProteinsColorectal NeoplasmsDNA ReplicationGenomic InstabilityHumansMiceMRE11 Homologue ProteinTopoisomerase I InhibitorsAtaxia Telangiectasia Mutated ProteinsDNA Topoisomerases, Type IMembrane ProteinsMRE11 Homologue ProteinTEX264 protein, humanTopoisomerase I Inhibitorscolorectal cancerDNA repairDNA replicationgenome stabilitynucleophagyprotein degradationselective autophagyTEX264topoisomerase 1 cleavage complexzebrafish

Identifiers

PMID39265577

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.