ATAC-seq of 3 months old wild type and hepatocyte-specific ATF6 overexpression mice

Hepatocellular carcinoma (HCC) is the fastest growing cause of cancer-related mortality with limited therapies. While endoplasmic reticulum (ER)-stress and the unfolded protein response (UPR) are implicated in HCC, the involvement of the UPR-transducer activating transcription factor 6 alpha (ATF6a) remains unclear. We generated hepatocyte specific n-ATF6 overexpression transgenic mice via Cre-mediated recombination. At 3 months age, livers from the transgenic mice and their wild type controls were harvested for ATAC-sequencing. Overall design: In total 9 mice were included, 4 from wild type mice and 5 from ATF6 transgenic mice.

肝细胞癌（Hepatocellular carcinoma, HCC）是增速最快的癌症相关死亡病因，且可用治疗手段有限。尽管内质网应激（endoplasmic reticulum stress, ER-stress）与未折叠蛋白反应（unfolded protein response, UPR）已被证实与肝细胞癌存在关联，但作为UPR转导因子的激活转录因子6α（ATF6a）在其中的参与机制仍不明确。本研究通过Cre重组酶介导的重组技术，构建了肝细胞特异性过表达n-ATF6的转基因小鼠。在小鼠3月龄时，采集转基因小鼠及其野生型对照小鼠的肝脏样本，用于转座酶可及性测序（ATAC-sequencing）。实验设计：本研究共纳入9只小鼠，其中野生型对照组4只，ATF6转基因小鼠组5只。