ArticleJournal of virology2008
Kaposi's sarcoma-associated herpesvirus disrupts adherens junctions and increases endothelial permeability by inducing degradation of VE-cadherin.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 49 citations in OpenAlex.
- Article
- Evaluation of plasma alpha-1-antichymotrypsin as a marker for pulmonary Kaposi sarcoma.International journal of cancer · 2025Article
- Review
- VE-cadherin shedding in vitro and in patients with aortic aneurysm and dissection.Scientific reports · 2024Article
- Review
- MARCH family E3 ubiquitin ligases selectively target and degrade cadherin family proteins.PloS one · 2024Article
- Kaposi Sarcoma, a Trifecta of Pathogenic Mechanisms.Diagnostics (Basel, Switzerland) · 2022Review
- Article
- A CaMolecular cancer research : MCR · 2019Article
- Modulation of Angiogenic Processes by the Human Gammaherpesviruses, Epstein-Barr Virus and Kaposi's Sarcoma-Associated Herpesvirus.Frontiers in microbiology · 2019Review
- Endothelial cell SHP-2 negatively regulates neutrophil adhesion and promotes transmigration by enhancing ICAM-1-VE-cadherin interaction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- p120-catenin regulates VE-cadherin endocytosis and degradation induced by the Kaposi sarcoma-associated ubiquitin ligase K5.Molecular biology of the cell · 2017Article
- SIRT1-mediated downregulation of p27Kip1 is essential for overcoming contact inhibition of Kaposi's sarcoma-associated herpesvirus transformed cells.Oncotarget · 2016Article
- KSHV-Mediated Angiogenesis in Tumor Progression.Viruses · 2016Review
- KSHV-Mediated Regulation of Par3 and SNAIL Contributes to B-Cell Proliferation.PLoS pathogens · 2016Article
- Connections matter--how viruses use cell–cell adhesion components.Journal of cell science · 2015Review
- Fbxo45 inhibits calcium-sensitive proteolysis of N-cadherin and promotes neuronal differentiation.The Journal of biological chemistry · 2014Article
- Phosphorylation of Kaposi's sarcoma-associated herpesvirus processivity factor ORF59 by a viral kinase modulates its ability to associate with RTA and oriLyt.Journal of virology · 2013Article
- Article
- Human tumour viruses and the deregulation of cell polarity in cancer.Nature reviews. Cancer · 2012Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 5 countries.
Funding
Abstract
Kaposi's sarcoma (KS) is a vascular tumor of proliferative endothelial cells caused by KS-associated herpesvirus (KSHV) infection. Aberrant vascular permeability is a hallmark of KS manifested as multifocal edematous skin and visceral lesions with dysregulated angiogenesis and vast inflammatory infiltrations. In this study, we showed that KSHV infection increased the permeability of confluent endothelial monolayers to serum albumin, blood-derived cells, KSHV-infected cells, and KSHV virions. KSHV-induced permeability was associated with the disruption of adherens junctions and the degradation of vascular endothelial cadherin (VE-cadherin) protein. Both the inactivation of KSHV virions by UV irradiation and the blockage of de novo protein synthesis with cycloheximide failed to reverse the KSHV-induced disruption of adherens junctions. However, soluble heparin that blocked KSHV entry into cells completely inhibited KSHV-induced permeability. Furthermore, the KSHV-induced degradation of VE-cadherin was dose dependent on the internalized virus particles. Together, these results indicate that KSHV infection induces vascular permeability by inducing VE-cadherin degradation during virus entry into cells. KSHV-induced aberrant vascular permeability could facilitate virus spread, promote inflammation and angiogenesis, and contribute to the pathogenesis of KSHV-induced malignancies.
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What OpenQuestion holds
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.