Joris Pothof

This study investigates how XPG function is regulated during nucleotide excision repair through dynamic interactions with TFIIH, XPA, and EXO1, revealing mechanisms of XPG recruitment and dissociation from DNA damage.

The paper develops a mathematical model to describe transcription loss due to accumulated DNA damage and analyzes its asymptotic behavior and first hitting time using mice data.

The paper shows that NER deficiency increases Signature 8 mutations in specific tissues and suggests this could be a biomarker for NER-deficiency in cancer.