The MAP kinase-activated protein kinase 2 (MK2) contributes to the Shiga toxin-induced inflammatory response.

ABSTRACT: Infection with Shiga toxin (STx)-producing bacteria can progress to a toxemic, extraintestinal injury cascade known as haemolytic uremic syndrome (HUS), the leading cause of acute renal failure in children. Mounting evidence suggests that STx activates stress response pathways in susceptible cells and has implicated the p38 mitogen-activated protein kinase (MAPK) pathway. More importantly, some of the pathology associated with HUS is believed to be a result of a STx-induced inflammatory response. From a siRNA screen of the human kinome adapted to a high-throughput format, we found that knock-down of the MAPK-activated protein kinase 2 (MK2), a downstream target of the p38 MAPK, protected against Shiga toxicity. Further characterization of the in vitro role of MK2 revealed that STx activate

SUBMITTER: Saenz JB 

PROVIDER: S-EPMC2859110 | biostudies-literature | 2010 Apr

REPOSITORIES: biostudies-literature