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Role for p53 in gene induction by double-stranded RNA
B T Hummer1, X L Li, B A Hassel
1Greenebaum Cancer Center, The University of Maryland, Baltimore, Maryland 21201, USA.
Journal of Virology
|July 20, 2001
Summary
The tumor suppressor p53 induces the interferon-stimulated gene 15 (ISG15). While p53 is crucial for double-stranded RNA (dsRNA) responses, viruses can trigger ISG15 independently of p53, indicating distinct signaling routes.
Area of Science:
- Molecular Biology
- Immunology
- Cellular Stress Response
Background:
- The tumor suppressor p53 plays a critical role in cellular responses to stress.
- Interferon-regulated pathways are involved in gene expression following biologic and genotoxic insults.
- Cross-talk between p53 and interferon pathways is known to influence gene induction.
Purpose of the Study:
- To investigate the relationship between p53 and interferon-stimulated genes (ISGs).
- To determine the role of p53 in the induction of ISG15 by various stimuli.
- To elucidate the signaling pathways utilized by different inducers of ISG15.
Main Methods:
- Western blotting to detect protein levels.
- RNA interference (RNAi) to deplete p53.
- Stimulation of cells with interferon, double-stranded RNA (dsRNA), and viral infection.
Main Results:
- The interferon-stimulated gene 15 (ISG15) is induced by p53.
- p53 is essential for optimal ISG15 induction by dsRNA.
- Interferon-induced ISG15 expression does not require p53.
- Viral infection induces ISG15 even in the absence of p53.
Conclusions:
- p53 directly regulates the expression of ISG15.
- Distinct signaling mechanisms are employed by viruses and dsRNA for ISG15 induction.
- The findings highlight the complex interplay between p53 and interferon-mediated immunity.