Loss of Activating Transcription Factor 3 reveals a distinct gene expression program modulating cell organization during pancreatitis.

ABSTRACT: Pancreatitis is triggered by environmental or cellular stress and is the leading contributor to pancreatic ductal adenocarcinoma. Altered gene expression in response to acinar cell stress determines the severity and duration of pancreatitis. However, it is unclear what factors contribute to this phenomenon. Here, we define a novel role for Activating Transcription Factor 3 (ATF3) during pancreatic injury. ATF3, a key mediator in the unfolded protein response, is robustly expressed in acinar cells during pancreatitis. Targeted deletion of Atf3 altered the molecular response to injury, with Atf3-/- acinar cells maintaining cell organization in response to cerulein, a well-established inducer of pancreatitis. Characterization of the mechanism using chromatin immunoprecipitation followed by

ORGANISM(S): Mus musculus

SUBMITTER: Christopher Pin 

PROVIDER: E-GEOD-60250 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress