1995
DOI: 10.1128/jvi.69.10.6389-6399.1995
|View full text |Cite
|
Sign up to set email alerts
|

Sequential activation of cyclin E and cyclin A gene expression by human papillomavirus type 16 E7 through sequences necessary for transformation

Abstract: To investigate E7-dependent biochemical changes which are involved in cellular transformation, we analyzed the influence of human papillomavirus type 16 (HPV-16) E7 on the expression of cell cycle regulatory proteins. Expression of E7 in established rodent fibroblasts (NIH 3T3), which was shown to be sufficient for transformation of these cells, leads to constitutive expression of the cyclin E and cyclin A genes in the absence of external growth factors. Surprisingly, expression of the cyclin D1 gene, which en… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

1
59
1
12

Year Published

1996
1996
2015
2015

Publication Types

Select...
9

Relationship

0
9

Authors

Journals

citations
Cited by 165 publications
(73 citation statements)
references
References 60 publications
1
59
1
12
Order By: Relevance
“…Inactivation of pRb, a negative regulator of the cyclin‐dependant kinase inhibitor p16, leads to p16 upregulation 16, 40, 41. E7 is able to elude the normally inhibitory effects of p16 by stimulating the S‐phase genes cyclin E and cyclin A 42, 43. This ultimately leads to the inactivation of checkpoints and regulatory pathways that transform the cells 44.…”
Section: Hpv Virology and Oncogenesismentioning
confidence: 99%
See 1 more Smart Citation
“…Inactivation of pRb, a negative regulator of the cyclin‐dependant kinase inhibitor p16, leads to p16 upregulation 16, 40, 41. E7 is able to elude the normally inhibitory effects of p16 by stimulating the S‐phase genes cyclin E and cyclin A 42, 43. This ultimately leads to the inactivation of checkpoints and regulatory pathways that transform the cells 44.…”
Section: Hpv Virology and Oncogenesismentioning
confidence: 99%
“…Loss of negative feedback as a result of downregulated pRb leads to upregulation of p16 16, 40, 41. Actions of E7 also allow for evasion of the normal tumor suppressor effects of p16 42, 43. These actions collectively result in the inactivation of apoptotic pathways, disruption in the cell cycle, and activation of cellular proliferation that leads to oncogenesis 16, 17, 43, 84, 85.…”
Section: The Role Of Hpv In Head and Neck Cancermentioning
confidence: 99%
“…First, as for E2f1-3, pocket proteins negatively regulate Cyclin E transcription, and their disruption leads to increased Cyclin E expression even in quiescent cells. 54,[67][68][69] Second, pocket proteins are phosphorylated by CYCLIN E:CDK 2 complexes at the conclusion of G 1 , leading to disruption of their E2F binding. 5 Third, Cyclin E is a direct transcriptional target of E2F1; mutation of two canonical, promoter-proximal E2F binding sites results in qualitatively similar temporal dynamics in response to serum but with a premature peak and overall elevated levels.…”
Section: Andmentioning
confidence: 99%
“…Thus, (i) in Drosophila, genetic studies indicate that cyclin E is the limiting downstream target of an E2F-mediated transactivating event (Duronio et al, 1995(Duronio et al, , 1998. (ii) In mammalian cells in culture, the disruption of E2F-pocket protein repressor complexes by viral oncoproteins adenovirus E1A (AdE1A) or herpesvirus 16 E7 (HPV16 E7) leads to a rapid induction of the endogenous cyclin E gene (Spitkovski et al, 1994;Zerfass et al, 1995). The same rapid induction is also observed following E2F1 overexpression Othani et al, 1995;Botz et al, 1996;Geng et al, 1996).…”
Section: Introductionmentioning
confidence: 99%