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

The Human Papillomavirus Type 8 E6 Protein Interferes with NOTCH Activation during Keratinocyte Differentiation

31 Jan 2013

Abstract excerpt

Cutaneous β-human papillomavirus (β-HPV) E6 proteins inhibit NOTCH signaling by associating with the transcriptional coactivator MAML1. NOTCH has tumor suppressor activities in epithelial cells and is activated during keratinocyte differentiation. Here we report that HPV type 8 (HPV8) E6 subverts NOTCH activation during keratinocyte differentiation by inhibiting RBPJ/MAML1 transcriptional activator complexes at...

Read the complete abstract on PubMed

Topics

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

Share to Cervical Cancer and HPV Research
Share to Immunotherapy and Immune Responses
Share to Viral-associated cancers and disorders

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 23365452
DOI: 10.1128/jvi.02527-12

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The Human Papillomavirus Type 8 E6 Protein Interferes with NOTCH Activation during Keratinocyte DifferentiationPMID 23365452Read ↗

Cutaneous β-human papillomavirus E6 proteins bind Mastermind-like coactivators and repress Notch signalingSemantic proximity Read ↗

The HPV8 E6 protein targets the Hippo and Wnt signaling pathways as part of its arsenal to restrain keratinocyte differentiationSemantic proximity Read ↗

Modulation of epithelial homeostasis by HPV using Notch and WntSemantic proximity Read ↗

Cutaneous HPV8 and MmuPV1 E6 Proteins Target the NOTCH and TGF-β Tumor Suppressors to Inhibit Differentiation and Sustain Keratinocyte ProliferationSemantic proximity Read ↗

Modulation of basal cell fate during productive and transforming HPV‐16 infection is mediated by progressive E6‐driven depletion of NotchSemantic proximity Read ↗

Inhibition of TGF-β and NOTCH Signaling by Cutaneous PapillomavirusesSemantic proximity Read ↗

Human Papillomavirus Type 16 E6 Amino Acid 83 Variants Enhance E6-Mediated MAPK Signaling and Differentially Regulate Tumorigenesis by Notch Signaling and Oncogenic RasSemantic proximity Read ↗

Downregulation of Toll-Like Receptor 9 Expression by Beta Human Papillomavirus 38 and Implications for Cell Cycle ControlSemantic proximity Read ↗

Complementation of Human Papillomavirus Type 16 E6 and E7 by Jagged1-Specific Notch1-Phosphatidylinositol 3-Kinase Signaling Involves Pleiotropic Oncogenic Functions Independent of CBF1;Su(H);Lag-1 ActivationSemantic proximity Read ↗

HPV16 E6 and E7 oncoproteins regulate Notch‐1 expression and cooperate to induce transformationSemantic proximity Read ↗

High-Risk Human Papillomaviruses Repress Constitutive Kappa Interferon Transcription via E6 To Prevent Pathogen Recognition Receptor and Antiviral-Gene ExpressionSemantic proximity Read ↗

Human papillomavirus 16 E2 regulates keratinocyte gene expression relevant to cancer and the viral life cycleSemantic proximity Read ↗

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