ReviewOncogene2001
Cell transformation by the middle T-antigen of polyoma virus.
Review in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 93 citations in OpenAlex.
- Recent advances in discovery and functional analysis of the small proteins and microRNA expressed by polyomaviruses.Virology · 2025Review
- Article
- Investigating the Role of Heparanase in Breast Cancer Development Utilising the MMTV-PyMT Murine Model of Mammary Carcinoma.Cancers · 2023Article
- Roads to Stat3 Paved with Cadherins.Cells · 2022Review
- Article
- Expression of novel proteins by polyomaviruses and recent advances in the structural and functional features of agnoprotein of JC virus, BK virus, and simian virus 40.Journal of cellular physiology · 2019Review
- PI3k and Stat3: Oncogenes that are Required for Gap Junctional, Intercellular Communication.Cancers · 2019Review
- Human polyomaviruses and cancer: an overview.Clinics (Sao Paulo, Brazil) · 2018Review
- Overexpression of MUC1 and Genomic Alterations in Its Network Associate with Prostate Cancer Progression.Neoplasia (New York, N.Y.) · 2017Article
- A Transformation-Defective Polyomavirus Middle T Antigen with a Novel Defect in PI3 Kinase Signaling.Journal of virology · 2017Article
- Article
- Transformation by Polyomavirus Middle T Antigen Involves a Unique Bimodal Interaction with the Hippo Effector YAP.Journal of virology · 2016Article
- Luminal epithelial cells within the mammary gland can produce basal cells upon oncogenic stress.Oncogene · 2016Article
- Tumor microenvironment regulates metastasis and metastasis genes of mouse MMTV-PymT mammary cancer cells in vivo.Veterinary pathology · 2014Article
- Expression of a phosphorylated substrate domain of p130Cas promotes PyMT-induced c-Src-dependent murine breast cancer progression.Carcinogenesis · 2013Article
- The HPV16 E6 oncoprotein causes prolonged receptor protein tyrosine kinase signaling and enhances internalization of phosphorylated receptor species.PLoS pathogens · 2013Article
- The p110α and p110β isoforms of PI3K play divergent roles in mammary gland development and tumorigenesis.Genes & development · 2012Article
- Integrin signaling in mammary epithelial cells and breast cancer.ISRN oncology · 2012Article
- ErbB3 ablation impairs PI3K/Akt-dependent mammary tumorigenesis.Cancer research · 2011Article
- Shp2 suppresses PyMT-induced transformation in mouse fibroblasts by inhibiting Stat3 activity.Virology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The polyoma virus region expressed early in the lytic cycle encodes three proteins, or T-antigens, that together cause the infected cell to enter the cell cycle and so provide a suitable cellular environment for replication of the viral genome. Under some circumstances infection does not kill the cell, but the T-antigens are still produced, resulting in the cell becoming transformed and tumorigenic. Most of this transforming action is exerted by the middle T-antigen, which has the ability to convert established cell lines to an oncogenic state. Middle T is a membrane bound polypeptide that interacts with a number of the proteins used by tyrosine kinase associated receptors to stimulate mitogenesis, so MT can be considered as a permanently active analogue of a receptor. Through a defined series of interactions, MT assembles a large multi-protein complex at the cell membrane, consisting of MT, the core dimer of protein phosphatase 2A, an src-family tyrosine kinase, and via phosphotyrosines, ShcA, phosphatidylinositol (3') kinase, and phospholipase Cgamma-1. Tyrosine phosphorylation stimulates PI3K and PLCgamma-1 enzymatic activity, and on ShcA creates binding sites for Grb2 with its associated Sos1 and Gab1. This activates p21(ras), and hence, the MAP kinase cascade. Consequently, MT can be used as a model for studying cell transformation and growth factor receptor signalling pathways.
Indexed as
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What OpenQuestion holds
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.