ArticleJournal of virology2011
Phosphorylation and polyubiquitination of transforming growth factor beta-activated kinase 1 are necessary for activation of NF-kappaB by the Kaposi's sarcoma-associated herpesvirus G protein-coupled receptor.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 29 citations in OpenAlex.
- Manipulation of Nuclear-Related Pathways During Kaposi's Sarcoma-Associated Herpesvirus Lytic Replication.Viruses · 2025Review
- Modulation of Lymphotoxin β Surface Expression by Kaposi's Sarcoma-Associated Herpesvirus K3 Through Glycosylation Interference.Journal of medical virology · 2025Article
- Review
- Review
- The interplay between EBV and KSHV viral products and NF-κB pathway in oncogenesis.Infectious agents and cancer · 2020Review
- Bioinformatics analysis of key biomarkers and pathways in KSHV infected endothelial cells.Medicine · 2019Article
- The regulatory role of protein phosphorylation in human gammaherpesvirus associated cancers.Virologica Sinica · 2017Review
- Porcine reproductive and respiratory syndrome virus (PRRSV) up-regulates IL-8 expression through TAK-1/JNK/AP-1 pathways.Virology · 2017Article
- Hijacking GPCRs by viral pathogens and tumor.Biochemical pharmacology · 2016Review
- MicroRNA-34a promotes genomic instability by a broad suppression of genome maintenance mechanisms downstream of the oncogene KSHV-vGPCR.Oncotarget · 2016Article
- Recent advances on viral manipulation of NF-κB signaling pathway.Current opinion in virology · 2015Review
- Oncovirus Kaposi sarcoma herpesvirus (KSHV) represses tumor suppressor PDLIM2 to persistently activate nuclear factor κB (NF-κB) and STAT3 transcription factors for tumorigenesis and tumor maintenance.The Journal of biological chemistry · 2015Article
- Kaposi's sarcoma-associated herpesvirus induces Nrf2 during de novo infection of endothelial cells to create a microenvironment conducive to infection.PLoS pathogens · 2014Article
- HIV-1 Vpr stimulates NF-κB and AP-1 signaling by activating TAK1.Retrovirology · 2014Article
- Helicobacter pylori activates NF-κB by inducing Ubc13-mediated ubiquitination of lysine 158 of TAK1.Journal of cellular biochemistry · 2013Article
- Genetic parameters and genome-wide association study of hyperpigmentation of the visceral peritoneum in chickens.BMC genomics · 2013Article
- Kaposi's sarcoma-associated herpesvirus G-protein-coupled receptor prevents AU-rich-element-mediated mRNA decay.Journal of virology · 2012Article
- Article
- The cytoplasmic domain of the HIV-1 glycoprotein gp41 induces NF-κB activation through TGF-β-activated kinase 1.Cell host & microbe · 2012Article
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) G protein-coupled receptor (vGPCR) protein has been shown to induce several signaling pathways leading to the modulation of host gene expression. The hijacking of these pathways facilitates the viral life cycle and leads to tumorigenesis. In the present work, we show that transforming growth factor β (TGF-β)-activated kinase 1 (TAK1) is an important player in NF-κB activation induced by vGPCR. We observed that the expression of an inactive TAK1 kinase mutant (TAK1M) reduces vGPCR-induced NF-κB nuclear translocation and transcriptional activity. Consequently, the expression of several NF-κB target genes normally induced by vGPCR was blocked by TAK1M expression, including interleukin 8 (IL-8), Gro1, IκBα, COX-2, cIAP2, and Bcl2 genes. Similar results were obtained after downregulation of TAK1 by small interfering RNA (siRNA) technology. The expression of vGPCR recruited TAK1 to the plasma membrane, and vGPCR interacts with TAK1. vGPCR expression also induced TAK1 phosphorylation and lysine 63-linked polyubiquitination, the two markers of the kinase's activation. Finally, inhibition of TAK1 by celastrol inhibited vGPCR-induced NF-κB activation, indicating this natural compound could be used as a potential therapeutic drug against KSHV malignancies involving vGPCR.
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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.