ArticleProceedings of the National Academy of Sciences of the United States of America1994
Protein domains connect cell cycle stimulation directly to initiation of DNA replication.
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 22 papers.
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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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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- Article
- Multiple DNA damage signaling and repair pathways deregulated by simian virus 40 large T antigen.Journal of virology · 2010Article
- Role of the interaction between large T antigen and Rb family members in the oncogenicity of JC virus.Oncogene · 2006Review
- Activation of CREB/ATF sites by polyomavirus large T antigen.Journal of virology · 2005Article
- A novel motif in geminivirus replication proteins interacts with the plant retinoblastoma-related protein.Journal of virology · 2004Article
- A tumor host range selection procedure identifies p150(sal2) as a target of polyoma virus large T antigen.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Effect on polyomavirus T-antigen function of mutations in a conserved leucine-rich segment of the DnaJ domain.Journal of virology · 2001Article
- A geminivirus replication protein interacts with the retinoblastoma protein through a novel domain to determine symptoms and tissue specificity of infection in plants.The EMBO journal · 2000Article
- J domain-independent regulation of the Rb family by polyomavirus large T antigen.Journal of virology · 2000Article
- The retinoblastoma protein alters the phosphorylation state of polyomavirus large T antigen in murine cell extracts and inhibits polyomavirus origin DNA replication.Journal of virology · 1999Article
- Polyomavirus large T antigen binds the transcriptional coactivator protein p300.Journal of virology · 1999Article
- Polyomavirus large T antigen induces alterations in cytoplasmic signalling pathways involving Shc activation.Journal of virology · 1999Article
- Signaling from polyomavirus middle T and small T defines different roles for protein phosphatase 2A.Molecular and cellular biology · 1998Article
- Transient viral DNA replication and repression of viral transcription are supported by the C-terminal domain of the bovine papillomavirus type 1 E1 protein.Journal of virology · 1998Article
- The DnaJ domain of polyomavirus large T antigen is required to regulate Rb family tumor suppressor function.Journal of virology · 1997Article
- Phosphorylation sites in polyomavirus large T antigen that regulate its function in viral, but not cellular, DNA synthesis.Journal of virology · 1997Article
- Cyclin-dependent kinase regulation of the replication functions of polyomavirus large T antigen.Journal of virology · 1997Article
- Tiny T antigen: an autonomous polyomavirus T antigen amino-terminal domain.Journal of virology · 1997Article
- An N-terminal deletion mutant of simian virus 40 (SV40) large T antigen oligomerizes incorrectly on SV40 DNA but retains the ability to bind to DNA polymerase alpha and replicate SV40 DNA in vitro.Journal of virology · 1996Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Polyoma large T antigen (LT) is the only viral gene product required for viral DNA replication. LT can be divided into two domains, one N-terminal (NT) spanning residues 1-260 and one C-terminal (CT) comprising approximately residues 264-785. NT is known to immortalize primary cells in a manner dependent on binding of pRB/p107. Here a CT construct comprising residues 264-785 was shown to have independent function in DNA replication. CT is entirely sufficient for driving viral DNA replication in vivo in growing mouse cells at a level approaching that of full-length LT. In contrast, CT is strikingly deficient for replication in serum-starved cells. However, this deficiency can be complemented by coexpression of NT. BrdUrd incorporation in transfected, starved cells showed that NT was sufficient for inducing S phase, suggesting a mechanism for complementation. By contrast, CT was unable to induce S phase when tested in the same assay. NT also promotes phosphorylation of sites in CT that are likely to be important for replication. Other DNA tumor virus gene products such as adenovirus E1A 12S and human papillomavirus 16 E7 could also complement CT for replication. Although NT, E1A 12S, and E7 all bind the retinoblastoma gene product (pRB) and p107, genetic analysis demonstrates an additional function, independent of that binding, is responsible for complementation.
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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.