Arginyltransferase1 drives a mitochondria-dependent program to induce cell death.

ABSTRACT: Cell death regulation is essential for stress adaptation and/or signal response. Past studies have shown that eukaryotic cell death is mediated by an evolutionarily conserved enzyme, arginyltransferase1 (Ate1). The downregulation of Ate1, as seen in many types of cancer, prominently increases cellular tolerance to a variety of stress conditions. Conversely, in yeast and mammalian cells, Ate1 is elevated under acute oxidative stress conditions, and this change appears to be essential for triggering cell death. However, studies of Ate1 were conventionally focused on its function in inducing protein degradation via the N-end rule pathway in the cytosol, leading to an incomplete understanding of the role of Ate1 in cell death. Our recent investigation shows that Ate1 dually exists in the cytos

SUBMITTER: Kumar A 

PROVIDER: S-EPMC12357888 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature