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Growth arrest by induction of p53 in DNA damaged keratinocytes is bypassed by human papillomavirus 16 E7.

10 May 1994

Abstract excerpt

Cellular tumor suppressors p53 and Rb play an important role in controlling cell proliferation. Inactivation of these tumor suppressor proteins can occur by gene mutation or by association with oncoproteins from the small DNA tumor viruses. One function of p53 is in regulating cell cycle check-point control after DNA damage. To dissect the pathways by which p53 and Rb may act, the E6 and E7 oncogenes of human...

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PMID: 8183918
DOI: 10.1073/pnas.91.10.4382

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Related research

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Growth arrest by induction of p53 in DNA damaged keratinocytes is bypassed by human papillomavirus 16 E7.PMID 8183918Read ↗

Analysis of the p53-mediated G1 growth arrest pathway in cells expressing the human papillomavirus type 16 E7 oncoproteinSemantic proximity Read ↗

p53-dependent G1 arrest involves pRB-related proteins and is disrupted by the human papillomavirus 16 E7 oncoprotein.Semantic proximity Read ↗

Human papillomavirus 16 E6 expression disrupts the p53-mediated cellular response to DNA damage.Semantic proximity Read ↗

Abrogation of growth arrest signals by human papillomavirus type 16 E7 is mediated by sequences required for transformation.Semantic proximity Read ↗

Inactivation of both the Retinoblastoma Tumor Suppressor and p21 by the Human Papillomavirus Type 16 E7 Oncoprotein Is Necessary To Inhibit Cell Cycle Arrest in Human Epithelial CellsSemantic proximity Read ↗

Human Papillomavirus Oncoproteins E6 and E7 Independently Abrogate the Mitotic Spindle CheckpointSemantic proximity Read ↗

Human papillomavirus E6 proteins mediate resistance to interferon-induced growth arrest through inhibition of p53 acetylation.Semantic proximity Read ↗

Induction of apoptosis in human keratinocytes containing mutated p53 alleles and its inhibition by both the E6 and E7 oncoproteins.Semantic proximity Read ↗

The ability of human papillomavirus E6 proteins to target p53 for degradation in vivo correlates with their ability to abrogate actinomycin D-induced growth arrestSemantic proximity Read ↗

Cellular responses of HPV-positive cancer cells to genotoxic anti-cancer agents: Repression ofE6/E7-oncogene expression and induction of apoptosisSemantic proximity Read ↗

Human Papillomavirus Type 16 E6 and E7 Cause Polyploidy in Human Keratinocytes and Up-Regulation of G2-M-Phase ProteinsSemantic proximity Read ↗

Induction of pRb Degradation by the Human Papillomavirus Type 16 E7 Protein Is Essential To Efficiently Overcome p16 <sup>INK4a</sup> -Imposed G <sub>1</sub> Cell Cycle ArrestSemantic proximity Read ↗

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