Jingjing Wang, Wenjuan Li, Ran Wang, Jinglun Xue, Jinzhong Chen
Institute of Genetics, School of Life Sciences, Fudan University, Shanghai 200433, China.
Acta biochimica et biophysica Sinica 2013 FebInactivation of p53 is needed during adenovirus type 5 DNA replication. E1B55K, an adenovirus early protein, has been reported to interact with p53 and inhibit p53 transactivation. Previous studies have shown that adeno-associated virus (AAV) type 2 could reduce the transforming potential of adenovirus by rescuing p53 from adenovirus-mediated degradation, but the details are not clear yet. We detected the Rep78-p53 interaction by co-immunoprecipitation assay. The co-localization assay revealed that Rep78 inhibits E1B55K-mediated p53 nuclear exportation. However, Rep78 did not detectably influence p53 stability and could not relieve the transcriptional inactivation of p53, as E1B55K could not be replaced from the p53-E1B55K complex by Rep78. Our results reveal a new possible mechanism that AAV-2 Rep78 inhibits adenovirus 5 by relocalizing p53 in the nucleus, which may shed some light on the regulatory mechanism of AAV-2 on its helper virus, adenovirus.
Jingjing Wang, Wenjuan Li, Ran Wang, Jinglun Xue, Jinzhong Chen. Adeno-associated virus Rep78 restricts adenovirus E1B55K-mediated p53 nuclear exportation. Acta biochimica et biophysica Sinica. 2013 Feb;45(2):135-40
PMID: 23165746
View Full Text