ATM regulates a DNA damage response posttranscriptional RNA operon in lymphocytes.

ABSTRACT: Maintenance of genomic stability depends on the DNA damage response, a biologic 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 after DNA damage, but its influence on posttranscriptional gene expression has not been examined on a global level. We show that ionizing radiation 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 process. Numerous mR

SUBMITTER: Mazan-Mamczarz K 

PROVIDER: S-EPMC3062410 | biostudies-literature | 2011 Feb

REPOSITORIES: biostudies-literature