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

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

7 Jun 1994

Abstract excerpt

The cell cycle regulatory tumor suppressor proteins p53 and pRB are targeted for inactivation by several tumor viruses, including the high-risk types of human papillomaviruses (HPVs) via interactions of the HPV E6 and E7 oncoproteins with p53 and pRB, respectively. p53 plays a central role in a signal transduction pathway that mediates G1 arrest after DNA damage, though the mechanism by which G1 arrest occurs has...

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 About Contact Helena Bioinformatics

Source

Identifiers

PMID: 8202487
DOI: 10.1073/pnas.91.12.5320

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

p53-dependent G1 arrest involves pRB-related proteins and is disrupted by the human papillomavirus 16 E7 oncoprotein.PMID 8202487Read ↗

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

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

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 ↗

Diminished capacity for p53 in mediating a radiation-induced G1 arrest in established human tumor cell lines.Semantic proximity Read ↗

Human Papillomavirus Type 16 E6 Promotes Retinoblastoma Protein Phosphorylation and Cell Cycle ProgressionSemantic proximity Read ↗

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

Papillomavirus E2 induces senescence in HPV-positive cells via pRB- and p21(CIP)-dependent pathways.Semantic proximity Read ↗

Tumour suppressors, kinases and clamps: How p53 regulates the cell cycle in response to DNA damageSemantic proximity Read ↗

Loss of p53 induces M-phase retardation following G2 DNA damage checkpoint abrogation.Semantic proximity Read ↗

Functional consequences of directed mutations in human papillomavirus E6 proteins: abrogation of p53-mediated cell cycle arrest correlates with p53 binding and degradation in vitro.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 ↗

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