ArticleJournal of virology2020
A Conserved Amino Acid in the C Terminus of Human Papillomavirus E7 Mediates Binding to PTPN14 and Repression of Epithelial Differentiation.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Inhibition of high risk HPV31 E8^E2 repressor activity enables differentiation-independent genome amplification and E4 expression.PLoS pathogens · 2026Article
- Characterization of patient-derived HPV16 E6 and E7 variant alleles.Journal of virology · 2026Article
- Inactivation of the RB1 and PTPN14 tumor suppressors cooperatively enables the carcinogenic activity of the human papillomavirus E7 oncoprotein.bioRxiv : the preprint server for biology · 2026Article
- MmuPV1 E7 promotes phenotypes associated with "high-risk" HPV infection in mouse keratinocytes.Journal of virology · 2025Article
- HPV-driven cancers: a looming threat and the potential of CRISPR/Cas9 for targeted therapy.Virology journal · 2025Review
- Review
- HPV18 E7 inhibits LATS1 kinase and activates YAP1 by degrading PTPN14.bioRxiv : the preprint server for biology · 2024Article
- Structural analysis of PTPN21 reveals a dominant-negative effect of the FERM domain on its phosphatase activity.Science advances · 2024Article
- Epidermal growth factor receptor-dependent stimulation of differentiation by human papillomavirus type 16 E5.Virology · 2024Article
- Epstein-Barr virus LMP1 protein promotes proliferation and inhibits differentiation of epithelial cells via activation of YAP and TAZ.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- MmuPV1 E7's interaction with PTPN14 delays Epithelial differentiation and contributes to virus-induced skin disease.PLoS pathogens · 2023Article
- Systematic Analysis of IL-1 Cytokine Signaling Suppression by HPV16 Oncoproteins.Journal of virology · 2022Article
- HPV 16 E7 alters translesion synthesis signaling.Virology journal · 2022Article
- Review
- Two conserved amino acids differentiate the biology of high-risk and low-risk HPV E5 proteins.Journal of medical virology · 2022Article
- CRISPR-Cas9‒Based Genomic Engineering in Keratinocytes: From Technology to Application.JID innovations : skin science from molecules to population health · 2022Review
- YAP1 activation by human papillomavirus E7 promotes basal cell identity in squamous epithelia.eLife · 2022Article
- Human Papillomaviruses as Infectious Agents in Gynecological Cancers. Oncogenic Properties of Viral Proteins.International journal of molecular sciences · 2022Review
- Description of CRISPR-Cas9 development and its prospects in human papillomavirus-driven cancer treatment.Frontiers in immunology · 2022Review
- The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis.Viruses · 2021Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The human papillomavirus (HPV) E7 oncoprotein is a primary driver of HPV-mediated carcinogenesis. The E7 proteins from diverse HPVs bind to the host cellular nonreceptor protein tyrosine phosphatase type 14 (PTPN14) and direct it for degradation through the activity of the E7-associated host E3 ubiquitin ligase UBR4. Here, we show that a highly conserved arginine residue in the C-terminal domain of diverse HPV E7 mediates the interaction with PTPN14. We found that disruption of PTPN14 binding through mutation of the C-terminal arginine did not impact the ability of several high-risk HPV E7 proteins to bind and degrade the retinoblastoma tumor suppressor or activate E2F target gene expression. HPVs infect human keratinocytes, and we previously reported that both PTPN14 degradation by HPV16 E7 and PTPN14 CRISPR knockout repress keratinocyte differentiation-related genes. Now, we have found that blocking PTPN14 binding through mutation of the conserved C-terminal arginine rendered both HPV16 and HPV18 E7 unable to repress differentiation-related gene expression. We then confirmed that the HPV18 E7 variant that could not bind PTPN14 was also impaired in repressing differentiation when expressed from the complete HPV18 genome. Finally, we found that the ability of HPV18 E7 to extend the life span of primary human keratinocytes required PTPN14 binding. CRISPR/Cas9 knockout of PTPN14 rescued keratinocyte life span extension in the presence of the PTPN14 binding-deficient HPV18 E7 variant. These results support the model that PTPN14 degradation by high-risk HPV E7 leads to repression of differentiation and contributes to its carcinogenic activity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.