ArticleMolecular and cellular biology1998
Signaling from polyomavirus middle T and small T defines different roles for protein phosphatase 2A.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- PCTAIRE1 promotes mitotic progression and resistance against antimitotic and apoptotic signals.Journal of cell science · 2022Article
- A Transformation-Defective Polyomavirus Middle T Antigen with a Novel Defect in PI3 Kinase Signaling.Journal of virology · 2017Article
- The broken "Off" switch in cancer signaling: PP2A as a regulator of tumorigenesis, drug resistance, and immune surveillance.BBA clinical · 2016Review
- Article
- Polyomavirus interaction with the DNA damage response.Virologica Sinica · 2015Review
- Papillomavirus E7 oncoproteins share functions with polyomavirus small T antigens.Journal of virology · 2015Article
- The Interplay between PP2A and microRNAs in Leukemia.Frontiers in oncology · 2015Review
- Polyomavirus small T antigen interacts with yes-associated protein to regulate cell survival and differentiation.Journal of virology · 2014Article
- Protein phosphatase 2A regulates innate immune and proteolytic responses to cigarette smoke exposure in the lung.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
- Comparisons between murine polyomavirus and Simian virus 40 show significant differences in small T antigen function.Journal of virology · 2011Article
- Lessons in signaling and tumorigenesis from polyomavirus middle T antigen.Microbiology and molecular biology reviews : MMBR · 2009Review
- Lessons from polyoma middle T antigen on signaling and transformation: A DNA tumor virus contribution to the war on cancer.Virology · 2009Review
- Polyomavirus middle T antigen induces the transcription of osteopontin, a gene important for the migration of transformed cells.Journal of virology · 2008Article
- A RNA interference screen identifies the protein phosphatase 2A subunit PR55gamma as a stress-sensitive inhibitor of c-SRC.PLoS genetics · 2007Article
- Polyomavirus small T antigen controls viral chromatin modifications through effects on kinetics of virus growth and cell cycle progression.Journal of virology · 2007Article
- Independent contributions of polyomavirus middle T and small T to the regulation of early and late gene expression and DNA replication.Journal of virology · 2006Article
- Genetic analysis of the polyomavirus DnaJ domain.Journal of virology · 2005Article
- Signaling via Shc family adapter proteins.Oncogene · 2001Review
- Induction of p53-independent apoptosis by simian virus 40 small t antigen.Journal of virology · 2001Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Polyomavirus causes a broad spectrum of tumors as the result of the action of its early proteins. This work compares signaling from middle T antigen (MT), the major transforming protein, to that from small T antigen (ST). The abilities of MT mutants to promote cell cycle progression in serum-starved NIH 3T3 cells were compared. Transformation-defective mutants lacking association with SHC or with phosphatidylinositol 3-kinase (PI3-K) retained the ability to induce DNA synthesis as measured by bromodeoxyuridine incorporation. Only when both interactions were lost in the Y250F/Y315F double mutant was MT inactive. ST promoted cell cycle progression in a manner dependent on its binding of protein phosphatase 2A (PP2A). Since the Y250F/Y315F MT mutant was wild type for PP2A binding yet unable to promote cell cycle progression, while ST was capable of promoting cell cycle progression, these experiments revealed a functional difference in MT and ST signaling via PP2A. Assays testing the abilities of MT and ST to induce the c-fos promoter and to activate c-jun kinase led to the same conclusion. ST, but not Y250F/Y315F MT, was able to activate the c-fos promoter through its interaction with PP2A. In contrast, MT, but not ST, was able to activate c-jun kinase by virtue of its interaction with PP2A.
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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 Socratic graph.