Human cells deficient in transcription-coupled repair show prolonged activation of the Jun N-terminal kinase and increased sensitivity following cisplatin treatment

PurposeThe Jun N-terminal kinases (JNKs) are activated by many biological, physical, and chemical stimuli, including the chemotherapeutic agent cisplatin. The primary pathway that repairs cisplatin-DNA adducts is nucleotide excision repair (NER). Xeroderma pigmentosum (XP) cells from complementation group C (XP-C) are competent in the transcription-coupled repair (TCR) pathway of NER but deficient in global genomic repair (GGR), Cockayne’s …