ArticleVirology2015
Human papillomavirus 16E6 and NFX1-123 potentiate Notch signaling and differentiation without activating cellular arrest.
Article in Virology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- NFX1-123 is required for keratinocyte differentiation and HPV 16 DNA maintenance in early and persistent infection models.Journal of virology · 2026Article
- Canonical and non-canonical functions of the non-coding RNA component (TERC) of telomerase complex.Cell & bioscience · 2025Review
- The Modulation of Septic Shock: A Proteomic Approach.International journal of molecular sciences · 2024Article
- In vitro antineoplastic effects of MK0752 in HPV-positive head and neck squamous cell carcinoma.Journal of cancer research and clinical oncology · 2023Article
- NFX1-123: A potential therapeutic target in cervical cancer.Journal of medical virology · 2023Article
- Review
- An enhanced triple fluorescence flow-cytometry-based assay shows differential activation of the Notch signaling pathway by human papillomavirus E6 proteins.Scientific reports · 2022Article
- High expression of NFX1-123 in HPV positive head and neck squamous cell carcinomas.Head & neck · 2022Article
- Article
- Review
- The Notch Pathway: A Link Between COVID-19 Pathophysiology and Its Cardiovascular Complications.Frontiers in cardiovascular medicine · 2021Review
- Genes Regulated by HPV 16 E6 and High Expression of NFX1-123 in Cervical Cancers.OncoTargets and therapy · 2020Article
- HPV type 16 E6 and NFX1-123 augment JNK signaling to mediate keratinocyte differentiation and L1 expression.Virology · 2019Article
- NFX1-123 is highly expressed in cervical cancer and increases growth and telomerase activity in HPV 16E6 expressing cells.Cancer letters · 2019Article
- Article
- Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
High-risk human papillomavirus (HR HPV) oncoproteins bind host cell proteins to dysregulate and uncouple apoptosis, senescence, differentiation, and growth. These pathways are important for both the viral life cycle and cancer development. HR HPV16 E6 (16E6) interacts with the cellular protein NFX1-123, and they collaboratively increase the growth and differentiation master regulator, Notch1. In 16E6 expressing keratinocytes (16E6 HFKs), the Notch canonical pathway genes Hes1 and Hes5 were increased with overexpression of NFX1-123, and their expression was directly linked to the activation or blockade of the Notch1 receptor. Keratinocyte differentiation genes Keratin 1 and Keratin 10 were also increased, but in contrast their upregulation was only indirectly associated with Notch1 receptor stimulation and was fully unlinked to growth arrest, increased p21(Waf1/CIP1), or decreased proliferative factor Ki67. This leads to a model of 16E6, NFX1-123, and Notch1 differently regulating canonical and differentiation pathways and entirely uncoupling cellular arrest from increased differentiation.
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