Show simple item record

dc.contributor.authorKnight, Gillian L.
dc.contributor.authorPugh, Alice G.
dc.contributor.authorYates, Emma
dc.contributor.authorBell, Ian
dc.contributor.authorWilson, Regina
dc.contributor.authorMoody, Cary A.
dc.contributor.authorLaimins, Laimonis A.
dc.contributor.authorRoberts, Sally
dc.date.accessioned2013-03-20T15:02:42Z
dc.date.available2013-03-20T15:02:42Z
dc.date.issued2013-03-20
dc.identifier.citationA cyclin-binding motif in human papillomavirus type 18 (HPV18) E1^E4 is necessary for association with CDK–cyclin complexes and G2/M cell cycle arrest of keratinocytes, but is not required for differentiation-dependent viral genome amplification or L1 capsid protein expression 2011, 412 (1):196 Virologyen
dc.identifier.issn00426822
dc.identifier.doi10.1016/j.virol.2011.01.007
dc.identifier.urihttp://hdl.handle.net/10545/274327
dc.descriptionInvestigation into the effects the HPV E4 protein has in viral life cycleen
dc.description.abstractThe G2/M arrest function of human papillomavirus (HPV) E4 proteins is hypothesized to be necessary for viral genome amplification. Full-length HPV18 E1^E4 protein is essential for efficient viral genome amplification. Here we identify key determinants within a CDK-bipartite consensus recognition motif in HPV18 E1^E4 that are critical for association with active CDK–cyclin complexes and in vitro phosphorylation at the predicted CDK phosphorylation site (threonine 23). The optimal cyclin-binding sequence (43RRLL46) within this E4 motif is required for G2/M arrest of primary keratinocytes and correlates with cytoplasmic retention of cyclin B1, but not cyclin A. Disruption of this motif in the E4 ORF of HPV18 genomes, and the subsequent generation of stable cell lines in primary keratinocytes revealed that this motif was not essential for viral genome amplification or L1 capsid protein induction. We conclude that the HPV18 E4 G2/M arrest function does not play a role in early vegetative events.
dc.relation.urlhttp://linkinghub.elsevier.com/retrieve/pii/S0042682211000122en
dc.rightsArchived with thanks to Virologyen
dc.subjectHPVen
dc.subjectCervical canceren
dc.titleA cyclin-binding motif in human papillomavirus type 18 (HPV18) E1^E4 is necessary for association with CDK–cyclin complexes and G2/M cell cycle arrest of keratinocytes, but is not required for differentiation-dependent viral genome amplification or L1 capsid protein expression
dc.typeArticleen
dc.identifier.journalVirologyen
html.description.abstractThe G2/M arrest function of human papillomavirus (HPV) E4 proteins is hypothesized to be necessary for viral genome amplification. Full-length HPV18 E1^E4 protein is essential for efficient viral genome amplification. Here we identify key determinants within a CDK-bipartite consensus recognition motif in HPV18 E1^E4 that are critical for association with active CDK–cyclin complexes and in vitro phosphorylation at the predicted CDK phosphorylation site (threonine 23). The optimal cyclin-binding sequence (43RRLL46) within this E4 motif is required for G2/M arrest of primary keratinocytes and correlates with cytoplasmic retention of cyclin B1, but not cyclin A. Disruption of this motif in the E4 ORF of HPV18 genomes, and the subsequent generation of stable cell lines in primary keratinocytes revealed that this motif was not essential for viral genome amplification or L1 capsid protein induction. We conclude that the HPV18 E4 G2/M arrest function does not play a role in early vegetative events.


Files in this item

Thumbnail
Name:
Publisher version

This item appears in the following Collection(s)

Show simple item record