The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Inhibition of CDK activity and PCNA-dependent DNA replication by p21 is blocked by interaction with the HPV-16 E7 oncoprotein
Abstract
p21 inhibits cyclin-dependent kinase (CDK) activity and proliferating cell nuclear antigen (PCNA)-dependent DNA replication by binding to CDK/cyclin complexes and to PCNA through distinct domains. The human papillomavirus (HPV)-16 E7 oncoprotein (16E7) abrogated a DNA damage-induced cell cycle arrest in vivo, despite high levels of p21. Using cell lysates and purified proteins we show that 16E7 prevented p21 both from inhibiting CDK2/cyclin E activity and PCNA-dependent DNA replication, whereas the nononcogenic HPV-6 E7 had reduced effects. Inactivation of both inhibitory functions of p21 was attained through binding between 16E7 and sequences in the carboxy-terminal end of p21 that overlap with the PCNA-binding site and the second p21 cyclin-binding motif. These data imply that the carboxyl terminus of p21 simultaneously modulates both CDK activity and PCNA-dependent DNA replication and that a single protein, 16E7, can override this modulation to disrupt normal cell cycle control.
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“Although E7 expression increases p21Cip1 through protein stabilization [154,155,156], cdk2 remains active in HPV-E7-expressing cells [147,148,157]”
From The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis (2021) · cites this paper as [147]
In the citing paper
“HPV-16 E7 abrogates the inhibition of cdk2 activity by interacting with CKIs, p21Cip1 [147,148] and p27Kip1 [149]”
From The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis (2021) · cites this paper as [147]
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Metadata
- Authors
- Funk, J. O., Waga, S., Harry, J. B., Espling, E., Stillman, B., & Galloway, D. A.
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 1997-08-15
- Volume
- 11
- Issue
- 16
- Pages
- 2090-2100
- ISSN
- 0890-9369
- 1549-5477
- Cited by
- 419
- References
- 9
- Language
- en
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