Orchestration of Telomeres and DNA Repair Factors in Mammalian Cells

摘要: Loss of telomere homeostasis via chromosome-genomic instability might effectively promote tumour progression. Telomere function may have contrasting roles: inducing replicative senescence and promoting tumourigenesis these roles vary between cell types depending on the expression telomerase enzyme, level mutations induced, deficiency related DNA repair pathways. Earlier studies in yeast their recent extension to mammalian systems convincingly indicated a role for proteins maintenance. An alternative maintenance mechanism has been identified mouse embryonic stem cells lacking RNA unit (mTERC) which nontelomeric sequences adjacent existing short stretches repeats are amplified. Our quest identifying telomerase-independent or mechanisms involvement potential factors such Studies by us others shown association cells. Mice deficient DNA-break sensing molecule, PARP-1 (poly [ADP]-ribopolymerase), increased levels chromosomal associated with extensive shortening. Ku80 null showed shortening chromosome end fusions whereas Ku80+/− exhibited an intermediate This overview will focus mainly repair/recombination damage signalling molecules as PARP-1, DNA-PKcs, Ku70/80, XRCC4 ATM, we studying quite sometime. As is crucial genomic stability, our results likely provide new insights into regulatory impact instability, ageing formation.