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Updated: May 8, 2026
14:57
Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
SUMOylation of p53 mediates interferon activities
Laura Marcos-Villar1, José V Pérez-Girón, Jéssica M Vilas
1Departamento Biología Molecular y Celular; Centro Nacional de Biotecnología-CSIC; Madrid, Spain.
Cell Cycle (Georgetown, Tex.)
|August 23, 2013
Summary
Type I interferon signaling activates SUMOylation of the tumor suppressor p53, initiating cellular senescence and enhancing antiviral defense against viruses like VSV. This highlights SUMOylation
Area of Science:
- Immunology
- Molecular Biology
- Cellular Biology
Background:
- SUMOylation regulates host proteins in innate and intrinsic immunity.
- Type I interferon (IFN) response initiation is SUMO-dependent.
- The tumor suppressor p53 modulates IFN responses, including apoptosis and senescence.
Purpose of the Study:
- To investigate the role of p53 SUMOylation in IFN signaling and antiviral responses.
- To determine if IFN treatment affects p53 SUMOylation and cellular senescence.
- To examine the impact of p53 SUMOylation on viral replication.
Main Methods:
- IFN treatment of cells.
- Analysis of p53 SUMOylation levels.
- Assessment of cellular senescence induction.
- Vesicular stomatitis virus (VSV) infection models.
- Evaluation of viral replication control.
Main Results:
- IFN treatment increases p53 SUMOylation.
- IFN-induced cellular senescence is partially dependent on p53 SUMOylation.
- VSV infection induces p53 SUMOylation.
- p53 SUMOylation favors the control of VSV replication.
Conclusions:
- IFN signaling induces p53 SUMOylation.
- p53 SUMOylation activates cellular senescence programs.
- p53 SUMOylation contributes to the antiviral functions of interferon.
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