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

Human Papillomavirus Oncoproteins E6 and E7 Independently Abrogate the Mitotic Spindle Checkpoint

1 Feb 1998

Abstract excerpt

The E6 and E7 genes of the high-risk human papillomavirus (HPV) types encode oncoproteins, and both act by interfering with the activity of cellular tumor suppressor proteins. E7 proteins act by associating with members of the retinoblastoma family, while E6 increases the turnover of p53. p53 has been implicated as a regulator of both the G1/S cell cycle checkpoint and the mitotic spindle checkpoint. When...

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 Hedgehog Signaling Pathway Studies

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 9445009
DOI: 10.1128/jvi.72.2.1131-1137.1998

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Human Papillomavirus Oncoproteins E6 and E7 Independently Abrogate the Mitotic Spindle CheckpointPMID 9445009Read ↗

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

Abrogation of the Postmitotic Checkpoint Contributes to Polyploidization in Human Papillomavirus E7-Expressing CellsSemantic proximity Read ↗

p53-Independent Abrogation of a Postmitotic Checkpoint Contributes to Human Papillomavirus E6 -Induced PolyploidySemantic proximity Read ↗

Role of Cdk1 in the p53-Independent Abrogation of the Postmitotic Checkpoint by Human Papillomavirus E6Semantic proximity Read ↗

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

HPV16 E6 induces chromosomal instability due to polar chromosomes caused by E6AP-dependent degradation of the mitotic kinesin CENP-ESemantic proximity Read ↗

The human papillomavirus type 16 E6 and E7 oncoproteins cooperate to induce mitotic defects and genomic instability by uncoupling centrosome duplication from the cell division cycleSemantic proximity Read ↗

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

Human Papillomavirus Type 16 E7 Oncoprotein Can Induce Abnormal Centrosome Duplication through a Mechanism Independent of Inactivation of Retinoblastoma Protein Family MembersSemantic proximity Read ↗

Human papillomavirus type 16 E7 oncoprotein associates with E2F6.Semantic proximity Read ↗

Critical roles for non-pRb targets of human papillomavirus type 16 E7 in cervical carcinogenesis.Semantic proximity Read ↗

Human Papillomavirus E7 Protein Deregulates Mitosis via an Association with Nuclear Mitotic Apparatus Protein 1Semantic proximity Read ↗

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