ArticleOncogene2004
The Kaposi's sarcoma-associated herpesvirus K-bZIP protein represses transforming growth factor beta signaling through interaction with CREB-binding protein.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Human cytomegalovirus blocks canonical TGFβ signaling during lytic infection to limit induction of type I interferons.PLoS pathogens · 2021Article
- Proteomic approaches to investigate gammaherpesvirus biology and associated tumorigenesis.Advances in virus research · 2021Review
- The bZIP Proteins of Oncogenic Viruses.Viruses · 2020Review
- Human Cytomegalovirus miRNAs Regulate TGF-β to Mediate Myelosuppression while Maintaining Viral Latency in CD34Cell host & microbe · 2020Article
- Viruses as key modulators of the TGF-β pathway; a double-edged sword involved in cancer.Reviews in medical virology · 2018Review
- DNA Tumor Virus Regulation of Host DNA Methylation and Its Implications for Immune Evasion and Oncogenesis.Viruses · 2018Review
- Article
- Viral manipulation of the cellular sumoylation machinery.Cell communication and signaling : CCS · 2017Review
- The Role of HBZ in HTLV-1-Induced Oncogenesis.Viruses · 2016Review
- MicroRNA expression profiles in Kaposi's sarcoma.Pathology oncology research : POR · 2014Article
- A Kaposi's sarcoma-associated herpesvirus microRNA and its variants target the transforming growth factor β pathway to promote cell survival.Journal of virology · 2012Article
- Interplay between electrical activity and bone morphogenetic protein signaling regulates spinal neuron differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Leucine zipper domain is required for Kaposi sarcoma-associated herpesvirus (KSHV) K-bZIP protein to interact with histone deacetylase and is important for KSHV replication.The Journal of biological chemistry · 2012Article
- Kaposi's sarcoma-associated herpesvirus-encoded microRNA miR-K12-11 attenuates transforming growth factor beta signaling through suppression of SMAD5.Journal of virology · 2012Article
- Important Roles of Cellular MicroRNA miR-155 in Leukemogenesis by Human T-Cell Leukemia Virus Type 1 Infection.ISRN microbiology · 2012Article
- Caloric restriction reduced 1, 2-dimethylhydrazine-induced aberrant crypt foci and induces the expression of Sirtuins in colonic mucosa of F344 rats.Journal of carcinogenesis · 2012Article
- Article
- Histone demethylase JMJD2A regulates Kaposi's sarcoma-associated herpesvirus replication and is targeted by a viral transcriptional factor.Journal of virology · 2011Article
- Aurora A selective inhibitor MLN8237 suppresses the growth and survival of HTLV-1-infected T-cells in vitro.Cancer science · 2010Article
- JunB mediates enhancer/promoter activity of COL1A2 following TGF-beta induction.Nucleic acids research · 2009Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is involved in the pathogenesis of KS, primary effusion lymphoma, and multicentric Castleman's disease. K-bZIP, the protein encoded by the open reading frame K8 of KSHV, is a member of the basic region-leucine zipper family of transcription factors. We studied the mechanisms that underlie KSHV-induced oncogenesis by investigating whether K-bZIP perturbs signaling through transforming growth factor beta (TGF-beta), which inhibits proliferation of a wide range of cell types. K-bZIP repressed TGF-beta-induced, Smad-mediated transcriptional activity and antagonized the growth-inhibitory effects of TGF-beta. Since both K-bZIP and Smad are known to interact with CREB-binding protein (CBP), the effect of CBP on inhibition of Smad-mediated transcriptional activation by K-bZIP was examined. K-bZIP mutants, which lacked the CBP-binding site, could not repress TGF-beta-induced or Smad3-mediated transcriptional activity. Overexpression of CBP restored K-bZIP-induced inhibition of Smad3-mediated transcriptional activity. Competitive interaction studies showed that K-bZIP inhibited the interaction of Smad3 with CBP. These results suggest that K-bZIP, through its binding to CBP, disrupts TGF-beta signaling by interfering with the recruitment of CBP into transcription initiation complexes on TGF-beta-responsive elements. We propose a possibility that K-bZIP may contribute to oncogenesis through its ability to promote cell survival by repressing TGF-beta signaling.
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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.