ATM regulates a DNA damage response post-transcriptional RNA operon in lymphocytes

ABSTRACT: Maintenance of genomic stability depends on the DNA damage response (DDR), a biological barrier in early stages of cancer development. Failure of this response results in genomic instability and high predisposition toward lymphoma, as seen in patients with ataxia-telangiectasia mutated (ATM) dysfunction. ATM activates multiple cell cycle checkpoints and DNA repair following DNA damage, but its influence on posttranscriptional gene expression has not been examined on a global level. We show that ionizing radiation (IR) modulates the dynamic association of the RNA-binding protein HuR with target mRNAs in an ATM-dependent manner, potentially coordinating the genotoxic response as an RNA operon. Pharmacologic ATM inhibition and use of ATM-null cells revealed a critical role for ATM in this pro

ORGANISM(S): Homo sapiens

SUBMITTER: Kevin Becker 

PROVIDER: E-GEOD-25848 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress