E2F1 sumoylation as a protective cellular mechanism in oxidative stress response
Abstract
Cells need to cope with oxidative stress caused by oxygen free radicals from mitochondrial oxidative phosphorylation. We identify a role for E2F1 to halt cell cycle progression for cell survival upon oxidative stress. Oxidative stress induces sumoylation of E2F1, primarily at lysine 266, which specifically modulates E2F1 transcriptional activity to enhance cell cycle arrest for cell survival. Furthermore, we identify SENP3 as an E2F1-interacting partner and a desumoylating enzyme for E2F1. Oxidative stress inhibits the interaction between E2F1 and SENP3, and leads to accumulation of sumoylated E2F1. These data demonstrate that sumoylation of E2F1 is important for cell cycle arrest to provide cells the opportunity to cope with oxidative stress and survive.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Jun 15, 2020
- Source ID
- 10.1073/pnas.1921554117
Entities
People
- Fang-Tsyr Lin
- Gang Li
- Joshua D. Graves
- Kang Liu
- Weei-Chin Lin
- Yu-Ju Lee
Organizations
- Baylor College of Medicine
- Congressionally Directed Medical Research Programs
- National Cancer Institute
- National Institute of Diabetes and Digestive and Kidney Diseases