ArticleOncogene2001
The HPV-16 E7 oncoprotein binds Skip and suppresses its transcriptional activity.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- HPV-18 E7 Interacts with Elk-1 Leading to Elevation of the Transcriptional Activity of Elk-1 in Cervical Cancer.Biomolecules & therapeutics · 2022Article
- Repression of Memo1, a Novel Target of Human Papillomavirus Type 16 E7, Increases Cell Proliferation in Cervical Cancer Cells.Journal of virology · 2022Article
- The human papillomavirus oncoproteins: a review of the host pathways targeted on the road to transformation.The Journal of general virology · 2021Review
- The human papillomavirus E7 oncoprotein as a regulator of transcription.Virus research · 2017Review
- Expression and prognostic role of SKIP in human breast carcinoma.Journal of molecular histology · 2014Article
- AtSKIP functions as a mediator between cytokinin and light signaling pathway in Arabidopsis thaliana.Plant cell reports · 2014Article
- The papillomavirus E7 proteins.Virology · 2013Review
- The human papillomavirus type 16 E7 oncoprotein targets Myc-interacting zinc-finger protein-1.Virology · 2012Article
- MetastamiRs: non-coding MicroRNAs driving cancer invasion and metastasis.International journal of molecular sciences · 2012Review
- Article
- Xenopus skip modulates Wnt/beta-catenin signaling and functions in neural crest induction.The Journal of biological chemistry · 2010Article
- Overexpression of STAT3 in HPV-mediated cervical cancer in a north Indian population.Molecular and cellular biochemistry · 2009Article
- Genome wide expression analysis in HPV16 cervical cancer: identification of altered metabolic pathways.Infectious agents and cancer · 2007Article
- Modulation of apoptosis by human papillomavirus (HPV) oncoproteins.Archives of virology · 2006Review
- Activated Src abrogates the Myc requirement for the G0/G1 transition but not for the G1/S transition.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Regulation of human papillomavirus type 16 E7 activity through direct protein interaction with the E2 transcriptional activator.Journal of virology · 2006Article
- Examination of the pRb-dependent and pRb-independent functions of E7 in vivo.Journal of virology · 2005Article
- Skip interacts with the retinoblastoma tumor suppressor and inhibits its transcriptional repression activity.Nucleic acids research · 2002Article
- The critical protein interactions and structures that elicit growth deregulation in cancer and viral replication.Wiley interdisciplinary reviews. Systems biology and medicineReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E7 is the major transforming protein of human papillomavirus (HPV), which is implicated in the development of cervical cancer. The transforming activity of E7 has been attributed in part to its interaction with the retinoblastoma (Rb) tumour suppressor; however, the Rb interaction alone is not sufficient for transformation by E7. In a screen for cellular targets of HPV E7, we identified the Ski interacting protein, Skip, as a new interacting partner of E7. We show that HPV-16 E7 associates with Skip via sequences in its carboxy terminal region, and the evolutionarily conserved proline rich sequences (PRS) of the SNW domain of Skip. E7 functionally targets Skip in vivo and inhibits its transcriptional activation activity. Two transformation defective mutants of E7 were identified that failed both to bind Skip and to inhibit its transcriptional activity. These results suggest that inhibition of Skip function may contribute to cell transformation by HPV-16 E7.
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Registered trials
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.