DNA damage and transcription stress cause ATP-mediated redesign of metabolism and potentiation of anti-oxidant buffering

ERCC1 is involved in a number of DNA repair pathways including nucleotide excision repair. Here the authors showed that reduced transcription in Ercc1-deficient mouse livers and cells increases ATP levels, suppressing glycolysis and rerouting glucose into the pentose phosphate shunt that generates reductive stress.