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Showing 1–20 of 20 results
Advanced filters: Author: Hannes Lans Clear advanced filters

  • Hereditary nucleotide excision repair deficiencies cause different cancerous and progeroid disorders of which the exact etiology is not understood. This study finds that prolonged binding of DNA repair factor TFIIH to DNA damage contributes to a more severe phenotype caused by DNA repair deficiency.

    • Alba Muniesa-Vargas
    • Carlota Davó-Martínez
    • Hannes Lans
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-16

  • DNA damage sensors DDB2 and XPC are fundamental factors to initiate global genome nucleotide excision repair and protect DNA from mutagenesis. Here the authors reveal that ubiquitin and TFIIH-stimulated DDB2 dissociation promotes DNA damage handover to XPC in nucleotide excision repair.

    • Cristina Ribeiro-Silva
    • Mariangela Sabatella
    • Hannes Lans
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-14

  • Two new studies report mutations in FAN1 and three other genome-stability genes that tie the DNA damage response to progressive kidney failure and the dysfunction of several other organs. These findings provide clues to the underlying causes of tissue decline and may add a series of genes to the growing list of genome maintenance factors that protect against premature aging.

    • Hannes Lans
    • Jan H J Hoeijmakers
    News & Views
    Nature Genetics
    Volume: 44, P: 836-838

  • Transcription-blocking DNA lesions lead to transcription stress that is associated with neurodegeneration and accelerated ageing. Recent structural and other findings have clarified how different obstructing lesions are recognized and removed and shed new light on the causes of various pathologies of repair deficiencies.

    • Marjolein van Sluis
    • Camila Gonzalo-Hansen
    • Jurgen A. Marteijn
    Reviews
    Nature Reviews Molecular Cell Biology
    Volume: 27, P: 234-251

  • SWI/SNF genes are commonly found to be mutated in different cancers. Here the authors report that the remodelers BRM and BRG1 are necessary for efficient nucleotide excision repair by promoting the expression of TFIIH subunit GTF2H1.

    • Cristina Ribeiro-Silva
    • Özge Z. Aydin
    • Wim Vermeulen
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-14

  • The SUMO-targeted ubiquitin ligase RNF111 promotes K63-linked ubiquitylation of SUMOylated XPC after DNA damage. Here the authors show that RNF111 is responsible for sequential XPC ubiquitylation, and RNF111-mediated ubiquitylation promotes the release of XPC from damaged DNA after NER initiation.

    • Loes van Cuijk
    • Gijsbert J. van Belle
    • Jurgen A. Marteijn
    ResearchOpen Access
    Nature Communications
    Volume: 6, P: 1-10

  • RNA–DNA hybrids are immunogenic species that can aberrantly accumulate in the cytoplasm after R-loop processing, linking R-loop accumulation to cell death through the innate immune response.

    • Magdalena P. Crossley
    • Chenlin Song
    • Karlene A. Cimprich
    Research
    Nature
    Volume: 613, P: 187-194

  • Nucleotide excision repair (NER) eliminates structurally diverse DNA lesions by repairing helix-distorting damage throughout the genome as well as transcription-blocking lesions. NER defects result in a wide range of disease phenotypes and recent findings have led to a mechanistic model that explains the complex genotype–phenotype correlations of transcription-coupled repair disorders.

    • Jurgen A. Marteijn
    • Hannes Lans
    • Jan H. J. Hoeijmakers
    Reviews
    Nature Reviews Molecular Cell Biology
    Volume: 15, P: 465-481

  • In certain premature-ageing syndromes, the architecture of the cell nucleus is abnormal. An animal model shows similar malformations during normal ageing, corroborating the idea that genome instability underlies ageing.

    • Hannes Lans
    • Jan H. J. Hoeijmakers
    News & Views
    Nature
    Volume: 440, P: 32-34

  • Hereditary mutations in TTDA/GTF2H5 cause a photosensitive form of the rare developmental disorder trichothiodystrophy, however the development of models has been hampered by mutations being lethal. Thijssen et al. show that deficiency of C. elegans TTDA ortholog GTF-2H5 is, compatible with life, in contrast to depletion of other TFIIH subunits and thus propose that this model could be used for studying the pathogenesis of trichothiodystrophy.

    • Karen L. Thijssen
    • Melanie van der Woude
    • Hannes Lans
    ResearchOpen Access
    Communications Biology
    Volume: 4, P: 1-12

  • Transcription-blocking DNA lesions (TBLs) cause transcription stress and are repaired by transcription-coupled nucleotide excision repair (TC-NER). TBL detection by the stalling of RNA polymerase II is highly efficient but may interfere with repair, and overall with transcription and replication. Consequently, TC-NER deregulation causes hereditary disorders with complex genotype–phenotype correlations.

    • Hannes Lans
    • Jan H. J. Hoeijmakers
    • Jurgen A. Marteijn
    Reviews
    Nature Reviews Molecular Cell Biology
    Volume: 20, P: 766-784