Abstract:
:HPV16 E6 deregulates G1/S cell cycle progression through p53 degradation preventing transcription of the CDK inhibitor p21(WAF1). However, additional mechanisms independent of p53 inactivation appear to exist. Here, we report that HPV16 E6 targets the cellular factor p150(Sal2), which positively regulates p21(WAF1) transcription. HPV16 E6 associates with p150(Sal2), inducing its functional inhibition by preventing its binding to cis elements on the p21(WAF1) promoter. A HPV16 E6 mutant, L110Q, which was unable to bind p150(Sal2), did not affect the ability of the cellular protein to bind p21(WAF1) promoter, underlining the linkage between these events. These data describe a novel mechanism by which HPV16 E6 induces cell cycle deregulation with a p53-independent pathway. The viral oncoprotein targets p150(Sal2), a positive transcription regulator of p21(WAF1) gene, preventing G1/S arrest and allowing cellular proliferation and efficient viral DNA replication.
journal_name
Virologyjournal_title
Virologyauthors
Parroche P,Touka M,Mansour M,Bouvard V,Thépot A,Accardi R,Carreira C,Roblot GG,Sylla BS,Hasan U,Tommasino Mdoi
10.1016/j.virol.2011.05.016subject
Has Abstractpub_date
2011-09-01 00:00:00pages
443-8issue
2eissn
0042-6822issn
1096-0341pii
S0042-6822(11)00251-0journal_volume
417pub_type
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