ArticleJournal of virology2004
Identification of TAZ as a binding partner of the polyomavirus T antigens.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
19 citing papers in PubMed, 31 citations in OpenAlex.
- A degradable form of polyoma small T antigen reveals the high specificity of TAZ in regulating gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- YAP1 activation by human papillomavirus E7 promotes basal cell identity in squamous epithelia.eLife · 2022Article
- The nonreceptor tyrosine kinase c-Src attenuates SCF(β-TrCP) E3-ligase activity abrogating Taz proteasomal degradation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- TAZ Induction Directs Differentiation of Thyroid Follicular Cells from Human Embryonic Stem Cells.Thyroid : official journal of the American Thyroid Association · 2017Article
- A Transformation-Defective Polyomavirus Middle T Antigen with a Novel Defect in PI3 Kinase Signaling.Journal of virology · 2017Article
- Transformation by Polyomavirus Middle T Antigen Involves a Unique Bimodal Interaction with the Hippo Effector YAP.Journal of virology · 2016Article
- The polyomavirus middle T-antigen oncogene activates the Hippo pathway tumor suppressor Lats in a Src-dependent manner.Oncogene · 2015Article
- Polyomavirus small T antigen interacts with yes-associated protein to regulate cell survival and differentiation.Journal of virology · 2014Article
- Protein phosphatase 2A isoforms utilizing Aβ scaffolds regulate differentiation through control of Akt protein.The Journal of biological chemistry · 2013Article
- Human tumour viruses and the deregulation of cell polarity in cancer.Nature reviews. Cancer · 2012Review
- TAZ induces growth factor-independent proliferation through activation of EGFR ligand amphiregulin.Cell cycle (Georgetown, Tex.) · 2012Article
- Regulation and function of the TAZ transcription co-activator.International journal of biochemistry and molecular biology · 2011Article
- Lessons in signaling and tumorigenesis from polyomavirus middle T antigen.Microbiology and molecular biology reviews : MMBR · 2009Review
- Cellular transformation by Simian Virus 40 and Murine Polyoma Virus T antigens.Seminars in cancer biology · 2009Review
- TEADs mediate nuclear retention of TAZ to promote oncogenic transformation.The Journal of biological chemistry · 2009Article
- Lessons from polyoma middle T antigen on signaling and transformation: A DNA tumor virus contribution to the war on cancer.Virology · 2009Review
- TAZ promotes cell proliferation and epithelial-mesenchymal transition and is inhibited by the hippo pathway.Molecular and cellular biology · 2008Article
- TAZ promotes PC2 degradation through a SCFbeta-Trcp E3 ligase complex.Molecular and cellular biology · 2007Article
- 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
5 authors at 1 institution in 1 country.
Funding
Abstract
A polyomavirus mutant isolated by the tumor host range selection procedure (19) has a three-amino-acid deletion (Delta2-4) in the common N terminus of the T antigens. To search for a cellular protein bound by wild-type but not the mutant T antigen(s), a yeast two-hybrid screen of a mouse embryo cDNA library was carried out with a bait of wild-type small T antigen (sT) fused N terminally to the DNA-binding domain of Gal4. TAZ, a transcriptional coactivator with a WW domain and PDZ-binding motif (17), was identified as a binding partner. TAZ bound in vivo to all three T antigens with different apparent affinities estimated as 1:7:100 (large T antigen [lT]:middle T antigen [mT]:sT). The Delta2-4 mutant T antigens showed no detectable binding. The sT and mT of the host range transformation-defective (hr-t) mutant NG59 with an alteration in the common sT/mT region (179 D-->NI) and a normal N terminus also failed to bind TAZ, while the unaltered lT bound but with reduced affinity compared to that seen in a wild-type virus infection. The WW domain but not the PDZ-binding motif of TAZ was essential for T antigen binding. The Delta2-4 mutant was defective in viral DNA replication. Forced overexpression of TAZ blocked wild-type DNA replication in a manner dependent on the binding site for the polyomavirus enhancer-binding protein 2alpha. Wild-type polyomavirus T antigens effectively block transactivation by TAZ. The functional significance of TAZ interactions with polyomavirus T antigens is discussed.
Indexed as
Identifiers
What Socratic 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 Socratic graph.