Abstract:
:The human papillomavirus type 16 E1--E4 protein is expressed abundantly in cells supporting viral DNA amplification, but its expression is lost during malignant progression. In cell culture, 16E1--E4 causes G2 cell cycle arrest by associating with and preventing the nuclear entry of Cdk1/cyclin B1 complexes. Here, we show that 16E1--E4 is also able to associate with cyclin A and Cdk2 during the G2 phase of the cell cycle. Only a weak association was apparent during S-phase, and progression through S-phase appeared unaffected. As with cyclin B1, the interaction of 16E1--E4 with cyclin A is dependent on residues T22/T23 and results in the accumulation of cyclin A in the cytoplasm where it colocalizes with 16E1--E4. 16E1--E4 serine 32 was found to be phosphorylated by Cdk2/cyclin A. We hypothesize that the interaction of 16E1--E4 with cyclin A may serve to increase the efficiency with which 16E1--E4 is able to prevent mitotic entry.
journal_name
Virologyjournal_title
Virologyauthors
Davy CE,Ayub M,Jackson DJ,Das P,McIntosh P,Doorbar Jdoi
10.1016/j.virol.2006.02.024subject
Has Abstractpub_date
2006-05-25 00:00:00pages
230-44issue
1eissn
0042-6822issn
1096-0341pii
S0042-6822(06)00099-7journal_volume
349pub_type
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