The puzzling regulation of the interferon signaling system by the p53 tumor suppressor protein.

ABSTRACT: The p53 tumor suppressor exhibits antiviral activity. The viral replication is also inhibited by interferons (IFNs), cytokines that regulate immune genes via STAT transcription factors. The best studied interferons belong to the type I (e.g., IFNα1) and type II (IFNγ) groups. IFNα1 and IFNγ induce the phosphorylation of STAT1 at Tyr701. Previously, we reported that p53 activates SOCS1, a negative regulator of STAT1 phosphorylation. Based on this, we hypothesized that p53, by activating SOCS1, reduces the phosphorylation of STAT1 and attenuates the activation of genes stimulated either by IFNα1 or IFNγ. To test this hypothesis, we exposed p53-proficient and p53-deficient cells to p53 activators along with either IFNα1 or IFNγ. We then assessed STAT1 phosphorylation and the expression of int

SUBMITTER: Bedzinska A 

PROVIDER: S-EPMC12165926 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature