ArticleOncogene2013
A20/TNFAIP3 inhibits NF-κB activation induced by the Kaposi's sarcoma-associated herpesvirus vFLIP oncoprotein.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Kaposi's Sarcoma: A Non-Communicable Outcome Mainly Prompted by Communicable Diseases in Sub-Saharan Africa.International journal of molecular sciences · 2025Review
- Review
- Kaposi's sarcoma herpesvirus viral FLICE inhibitory protein modulates A20 deubiquitinase activity.Access microbiology · 2024Article
- The genomic and molecular landscape of splenic marginal zone lymphoma, biological and clinical implications.Exploration of targeted anti-tumor therapy · 2024Review
- Cytotoxic CD4Med (New York, N.Y.) · 2023Article
- Article
- The interplay between EBV and KSHV viral products and NF-κB pathway in oncogenesis.Infectious agents and cancer · 2020Review
- KSHV: Immune Modulation and Immunotherapy.Frontiers in immunology · 2019Review
- The Role of Deubiquitinases in Oncovirus and Host Interactions.Journal of oncology · 2019Review
- CADM1 is essential for KSHV-encoded vGPCR-and vFLIP-mediated chronic NF-κB activation.PLoS pathogens · 2018Article
- Effects of DLC1 Deficiency on Endothelial Cell Contact Growth Inhibition and Angiosarcoma Progression.Journal of the National Cancer Institute · 2018Article
- C11orf95-RELA fusion present in a primary supratentorial ependymoma and recurrent sarcoma.Brain tumor pathology · 2015Article
- Review
- Biphasic regulation of A20 gene expression during human cytomegalovirus infection.Virology journal · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) K13/vFLIP (viral Flice-inhibitory protein) induces transcription of numerous genes through NF-κB activation, including pro-inflammatory cytokines, which contribute to the pathogenesis of Kaposi's sarcoma (KS). In this study, we report that KSHV vFLIP induces the expression of the NF-κB regulatory proteins A20, ABIN-1 and ABIN-3 (A20-binding NF-κB inhibitors) in primary human endothelial cells, and that KS spindle cells express A20 in KS tissue. In reporter assays, A20 strongly impaired vFLIP-induced NF-κB activation in 293T cells, but ABIN-1 and ABIN-3 did not. Mutational analysis established that the C-terminal domain (residues 427-790) is critical for A20 modulation of NF-κB, but the ubiquitin-editing OTU (ovarian tumor) domain is not. In functional assays, A20 inhibited vFLIP-induced expression of the chemokine IP-10, reduced vFLIP-induced cell proliferation and increased IKK1 protein levels. Thus, we demonstrate that A20 negatively regulates NF-κB activation directly induced by KSHV vFLIP. By attenuating excessive and prolonged vFLIP-induced NF-κB activation that could be harmful to KSHV-infected cells, A20 likely has an important role in the pathogenesis of KSHV-associated diseases, in which vFLIP is expressed.
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Registered trials
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