ArticleJournal of virology1998
Serine 257 phosphorylation regulates association of polyomavirus middle T antigen with 14-3-3 proteins.
Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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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
18 citing papers in PubMed, 40 citations in OpenAlex.
- Dielectric Signatures of Late Carcinoma Immune Cells Using MMTV-PyMT Mammary Carcinoma Models.ACS omega · 2024Article
- Cystatin C deficiency suppresses tumor growth in a breast cancer model through decreased proliferation of tumor cells.Oncotarget · 2017Article
- A Transformation-Defective Polyomavirus Middle T Antigen with a Novel Defect in PI3 Kinase Signaling.Journal of virology · 2017Article
- Article
- 14-3-3ζ as a prognostic marker and therapeutic target for cancer.Expert opinion on therapeutic targets · 2010Review
- 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
- 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
- Genetic analysis of the polyomavirus DnaJ domain.Journal of virology · 2005Article
- Dynamic interactions between 14-3-3 proteins and phosphoproteins regulate diverse cellular processes.The Biochemical journal · 2004Review
- Functional specificity in 14-3-3 isoform interactions through dimer formation and phosphorylation. Chromosome location of mammalian isoforms and variants.Plant molecular biology · 2002Review
- Review
- Natural biology of polyomavirus middle T antigen.Microbiology and molecular biology reviews : MMBR · 2001Review
- Expression of major capsid protein VP-1 in the absence of viral particles in thymomas induced by murine polyomavirus.Journal of virology · 2001Article
- Catalytically inactive protein phosphatase 2A can bind to polyomavirus middle tumor antigen and support complex formation with pp60(c-src).Journal of virology · 1999Article
- Association between src-kinases and the polyoma virus oncogene middle T-antigen requires PP2A and a specific sequence motif.Oncogene · 1999Article
- Signaling from polyomavirus middle T and small T defines different roles for protein phosphatase 2A.Molecular and cellular biology · 1998Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Polyomavirus middle T antigen (MT) is phosphorylated on serine residues. Partial proteolytic mapping and Edman degradation identified serine 257 as a major site of phosphorylation. This was confirmed by site-directed mutagenesis. Isoelectric focusing of immunoprecipitated MT from transfected 293T cells showed that phosphorylation on wild-type MT occurred at near molar stoichiometry at S257. MT was previously shown to be associated with 14-3-3 proteins, which have been connected to cell cycle regulation and signaling. The association of 14-3-3 proteins with MT depended on the serine 257 phosphorylation site. This has been demonstrated by comparing wild-type and S257A mutant MTs expressed with transfected 293T cells or with Sf9 cells infected with recombinant baculoviruses. The 257 site is not critical for transformation of fibroblasts in vitro, since S257A and S257C mutant MTs retained the ability to form foci or colonies in agar. The tumor profile of a virus expressing S257C MT showed a striking deficiency in the induction of salivary gland tumors. The basis for this defect is uncertain. However, differences in activity for the wild type and mutant MT lacking the 14-3-3 binding site have been observed in transient reporter assays.
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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.