Here we show that human cells lacking XRCC1 fail to rapidly recover transcription following DNA base damage, a phenotype also observed in patient-derived fibroblasts with XRCC1 mutations and Xrcc1 −/− mouse neurons. ![]() However, the mechanism(s) by which this toxic PARP1 activity triggers cellular dysfunction are unclear. Genetic defects in the repair of DNA single-strand breaks (SSBs) can result in neurological disease triggered by toxic activity of the single-strand-break sensor protein PARP1.
0 Comments
Leave a Reply. |