ArticleProceedings of the National Academy of Sciences of the United States of America1994
Polyomavirus middle-sized tumor antigen modulates c-Jun phosphorylation and transcriptional activity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Characterization of CADD522, a small molecule that inhibits RUNX2-DNA binding and exhibits antitumor activity.Oncotarget · 2017Article
- Merkel cell polyomavirus in Merkel cell carcinogenesis: small T antigen-mediates c-Jun phosphorylation.Virus genes · 2016Article
- DNA methyltransferase inhibitor, zebularine, delays tumor growth and induces apoptosis in a genetically engineered mouse model of breast cancer.Molecular cancer therapeutics · 2012Article
- Transgenic expression of polyomavirus middle T antigen in the mouse prostate gives rise to carcinoma.Journal of virology · 2011Article
- Jnk2 effects on tumor development, genetic instability and replicative stress in an oncogene-driven mouse mammary tumor model.PloS one · 2010Article
- 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
- Role of Zn2+ ions in host-virus interactions.Journal of virology · 2008Review
- 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
- ShcA tyrosine phosphorylation sites can replace ShcA binding in signalling by middle T-antigen.The EMBO journal · 2001Article
- Role of middle T-small T in the lytic cycle of polyomavirus: control of the early-to-late transcriptional switch and viral DNA replication.Journal of virology · 2001Article
- Natural biology of polyomavirus middle T antigen.Microbiology and molecular biology reviews : MMBR · 2001Review
- Middle T antigen activation of signal transduction pathways does not overcome p53-mediated growth arrest.Journal of virology · 1999Article
- Retinoic acid inhibits transformation by preventing phosphatidylinositol 3-kinase dependent activation of the c-fos promoter.Oncogene · 1999Article
- Signaling from polyomavirus middle T and small T defines different roles for protein phosphatase 2A.Molecular and cellular biology · 1998Article
- Multimerization of polyomavirus middle-T antigen.Journal of virology · 1997Article
- A novel 39-kilodalton membrane protein binds GTP in polyomavirus-transformed cells.Journal of virology · 1997Article
- Altered susceptibility to tumor necrosis factor alpha-induced apoptosis of mouse cells expressing polyomavirus middle and small T antigens.Journal of virology · 1997Article
- Dominant inhibitory Ras delays Sindbis virus-induced apoptosis in neuronal cells.Journal of virology · 1996Article
- AP1 enhances polyomavirus DNA replication by promoting T-antigen-mediated unwinding of DNA.Journal of virology · 1996Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Polyomavirus middle-sized tumor antigen (MT) increases the expression of c-jun through a phorbol 12-O-tetradecanoate 13-acetate response element in the c-jun promoter. To investigate the cellular signaling pathways affected by MT, we studied the role of the c-Ras and Raf-1 proteins in MT-induced transactivation of c-jun and cell transformation. There was an increase in GTP complexed to Ras in MT-expressing cells, indicating an increase in Ras activity. Coexpression of dominant inhibitory mutants of Ha-ras and raf-1 with MT inhibited MT-mediated transactivation and focus formation. Studies of the phosphorylation of c-Jun showed that MT expression increased the phosphorylation of Ser-63 and Ser-73 in the transactivation domain and decreased the phosphorylation of a peptide containing Ser-243, Ser-249, and Thr-231 in the DNA binding domain. MT increased the transcriptional activating ability of c-Jun but failed to increase the transcriptional activating ability of c-Jun mutants with Ser-63 and Ser-73 changed to nonphosphorylatable Ala, indicating that MT modulates c-Jun activity through phosphorylation. The dominant inhibitory mutants of Ha-ras and raf-1 interfered with the ability of MT to activate c-Jun. The results indicate that MT induces a phosphorylation cascade through the activation of c-Ras and Raf-1 and that c-Jun is one of the downstream targets that may cause changes in gene expression leading to cell transformation.
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