作者: Enrique Samper , Fermín A Goytisolo , Predrag Slijepcevic , Paul PW van Buul , María A Blasco
DOI: 10.1093/EMBO-REPORTS/KVD051
关键词:
摘要: Ku86 together with Ku70, DNA-PKcs, XRCC4 and DNA ligase IV forms a complex involved in repairing double-strand breaks (DSB) mammals. Yeast Ku has an essential role at the telomere; particular, deficiency leads to telomere shortening, loss of clustering, telomeric silencing deregulation G-overhang. In mammals, proteins associate repeats; however, possible regulating length not yet been addressed. We have measured different cell types from wild-type Ku86-deficient mice. contrast yeast, does result shortening or G-strand overhang. Interestingly, Ku86–/– cells show fusions long telomeres (>81 kb) fusion point. These results indicate that mammalian plays fundamental by preventing independently TTAGGG repeats integrity