Knockout of p53 leads to a significant increase in ALV-J replication.

ABSTRACT: Avian leukemia is a common malignant disease, and and its regulatory mechanism is complex. As the most extensive tumor suppressor gene in cancer research, p53 can control multiple functions such as that of DNA repair, induction of apoptosis, cell cycle arrest and so on. In view of the diversity associated with varied function of p53, this study analyzed the possible effect of gene on ALV-J replication and its regulatory mechanism. We successfully constructed a p53 knockout DF-1 cell line (p53-KO-DF-1 cells) by using CRISPR-Cas9 system. When ALV-J was co-infected with DF-1 and p53-KO-DF-1 cells, it was found that compared with wild-type DF-1 cells, the viral copy number of p53-KO-DF-1 cells infected with ALV-J increased significantly 48 h after infection, whereas the expression of innate im

SUBMITTER: Zhang H 

PROVIDER: S-EPMC8377548 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature