IRTKS Regulates MDM2-Mediated p53 Ubiquitination
Author Information
Author(s): Wang Ke-Sheng, Chen Gang, Shen Hai-Lian, Li Ting-Ting, Chen Fei, Wang Qin-Wan, Wang Zhi-Qin, Han Ze-Guang, Zhang Xin
Primary Institution: Shanghai-MOST Key Laboratory for Disease and Health Genomics, Chinese National Human Genome Center at Shanghai
Hypothesis
IRTKS modulates MDM2-mediated p53 ubiquitination in unstressed cells.
Conclusion
IRTKS enhances low levels of MDM2-mediated p53 ubiquitination, affecting p53's transcriptional activity.
Supporting Evidence
- IRTKS interacts directly with p53 and MDM2.
- IRTKS overexpression reduces p53-induced apoptosis.
- IRTKS enhances p53 ubiquitination at low levels of MDM2.
- DNA damage dissociates IRTKS from p53.
Takeaway
IRTKS helps control a protein called p53, which is important for stopping cancer, by changing how it is marked for destruction in cells.
Methodology
The study involved cell line experiments to assess the interaction between IRTKS, p53, and MDM2, including overexpression and knockdown techniques.
Statistical Information
P-Value
p<0.01
Statistical Significance
p<0.01
Digital Object Identifier (DOI)
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