Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Analysis of the p53-mediated G1 growth arrest pathway in cells expressing the human papillomavirus type 16 E7 oncoprotein

1 Apr 1997

Abstract excerpt

Cells expressing human papillomavirus type 16 (HPV-16) E7, similar to those which express HPV-16 E6, are resistant to a p53-mediated G1 growth arrest. We examined the p53-mediated DNA damage response pathway in E7-expressing cells to determine the mechanism by which E7-containing cells continue to cycle. In response to DNA damage, no dramatic difference was detected in G1- or S-phase cyclin or cyclin-dependent...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cancer-related Molecular Pathways
Share to Cervical Cancer and HPV Research
Share to Molecular Biology Techniques and Applications

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Identifiers

PMID: 9060648
DOI: 10.1128/jvi.71.4.2905-2912.1997

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Analysis of the p53-mediated G1 growth arrest pathway in cells expressing the human papillomavirus type 16 E7 oncoproteinPMID 9060648Read ↗

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

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 ↗

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

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

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

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

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

The E7 Oncoprotein of Human Papillomavirus Type 16 Stabilizes p53 through a Mechanism Independent of p19 ARFSemantic proximity Read ↗

Human Papillomavirus Type 16 E7 Maintains Elevated Levels of the cdc25A Tyrosine Phosphatase during Deregulation of Cell Cycle ArrestSemantic proximity Read ↗

Destabilization of the Retinoblastoma Tumor Suppressor by Human Papillomavirus Type 16 E7 Is Not Sufficient To Overcome Cell Cycle Arrest in Human KeratinocytesSemantic proximity Read ↗

Examination of the pRb-Dependent and pRb-Independent Functions of E7 In VivoSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.