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Wim Vermeulen

Researcher at Erasmus University Rotterdam

Publications -  195
Citations -  20592

Wim Vermeulen is an academic researcher from Erasmus University Rotterdam. The author has contributed to research in topics: Nucleotide excision repair & DNA repair. The author has an hindex of 74, co-authored 188 publications receiving 19121 citations. Previous affiliations of Wim Vermeulen include Centre national de la recherche scientifique & Erasmus University Medical Center.

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Understanding nucleotide excision repair and its roles in cancer and ageing

TL;DR: A mechanistic model is proposed that explains the complex genotype–phenotype correlations of transcription-coupled repair disorders and uncovered new aspects of DNA-damage detection by NER, how NER is regulated by extensive post-translated modifications, and the dynamic chromatin interactions that control its efficiency.
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DNA repair helicase: a component of BTF2 (TFIIH) basic transcription factor

TL;DR: Findings suggest that transcription and nucleotide excision repair may share common factors and hence may be considered to be functionally related.
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Sequential Assembly of the Nucleotide Excision Repair Factors In Vivo

TL;DR: XPC is identified as the earliest known NER factor in the reaction mechanism, insight is given into the order of subsequent NER components, evidence for a dual role of XPA is provided, and a concept of sequential assembly of repair proteins at the site of the damage rather than a preassembled repairosome is supported.
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ERCC6, a member of a subfamily of putative helicases, is involved in Cockayne's syndrome and preferential repair of active genes.

TL;DR: The characterization of ERCC6, a gene involved in preferential repair in eukaryotes, corrects the repair defect of CS complementation group B (CS-B), and encodes a protein of 1493 amino acids, containing seven consecutive domains conserved between DNA and RNA helicases.
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A new progeroid syndrome reveals that genotoxic stress suppresses the somatotroph axis

TL;DR: It is concluded that unrepaired cytotoxic DNA damage induces a highly conserved metabolic response mediated by the IGF1/insulin pathway, which re-allocates resources from growth to somatic preservation and life extension, and demonstrates that ageing and end-of-life fitness are determined both by stochastic damage and genetics.