ArticlePLoS pathogens2015
Inhibiting the Recruitment of PLCγ1 to Kaposi's Sarcoma Herpesvirus K15 Protein Reduces the Invasiveness and Angiogenesis of Infected Endothelial Cells.
Article in PLoS pathogens, 2015. 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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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- ORF57/MTA in KSHV Biology and Pathogenesis: Update From 2015.Journal of medical virology · 2026Review
- Modern Approach to Manage Patients With Kaposi Sarcoma.Journal of medical virology · 2025Review
- Membrane-bound Merkel cell polyomavirus middle T protein constitutively activates PLCγ1 signaling through Src-family kinases.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Cancers associated with human gammaherpesviruses.The FEBS journal · 2022Review
- Genome-wide regulation of KSHV RNA splicing by viral RNA-binding protein ORF57.PLoS pathogens · 2022Article
- Human Gammaherpesvirus 8 Oncogenes Associated with Kaposi's Sarcoma.International journal of molecular sciences · 2022Review
- Molecular Mechanisms of Kaposi Sarcoma Development.Cancers · 2022Article
- Recruitment of phospholipase Cγ1 to the non-structural membrane protein pK15 of Kaposi Sarcoma-associated herpesvirus promotes its Src-dependent phosphorylation.PLoS pathogens · 2021Article
- An endothelial cell line infected by Kaposi's sarcoma-associated herpes virus (KSHV) allows the investigation of Kaposi's sarcoma and the validation of novel viral inhibitors in vitro and in vivo.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Kaposi sarcoma.Nature reviews. Disease primers · 2019Review
- Modulation of Angiogenic Processes by the Human Gammaherpesviruses, Epstein-Barr Virus and Kaposi's Sarcoma-Associated Herpesvirus.Frontiers in microbiology · 2019Review
- Pathogenesis of Human Gammaherpesviruses: Recent Advances.Current clinical microbiology reports · 2019Article
- Quantitative RNAseq analysis of Ugandan KS tumors reveals KSHV gene expression dominated by transcription from the LTd downstream latency promoter.PLoS pathogens · 2018Article
- Kaposi's Sarcoma-Associated Herpesvirus Nonstructural Membrane Protein pK15 Recruits the Class II Phosphatidylinositol 3-Kinase PI3K-C2α To Activate Productive Viral Replication.Journal of virology · 2018Article
- Expression and Subcellular Localization of the Kaposi's Sarcoma-Associated Herpesvirus K15P Protein during Latency and Lytic Reactivation in Primary Effusion Lymphoma Cells.Journal of virology · 2017Article
- Kaposi sarcoma herpesvirus pathogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- The Kaposi's sarcoma-associated herpesvirus (KSHV) non-structural membrane protein K15 is required for viral lytic replication and may represent a therapeutic target.PLoS pathogens · 2017Article
- Modulation of oncogenic signaling networks by Kaposi's sarcoma-associated herpesvirus.Biological chemistry · 2017Review
- Manipulation of the host cell membrane by human γ-herpesviruses EBV and KSHV for pathogenesis.Virologica Sinica · 2016Review
- KSHV-Mediated Angiogenesis in Tumor Progression.Viruses · 2016Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaposi's sarcoma (KS), caused by Kaposi's sarcoma herpesvirus (KSHV), is a highly vascularised tumour of endothelial origin. KSHV infected endothelial cells show increased invasiveness and angiogenesis. Here, we report that the KSHV K15 protein, which we showed previously to contribute to KSHV-induced angiogenesis, is also involved in KSHV-mediated invasiveness in a PLCγ1-dependent manner. We identified βPIX, GIT1 and cdc42, downstream effectors of PLCγ1 in cell migration, as K15 interacting partners and as contributors to KSHV-triggered invasiveness. We mapped the interaction between PLCγ1, PLCγ2 and their individual domains with two K15 alleles, P and M. We found that the PLCγ2 cSH2 domain, by binding to K15P, can be used as dominant negative inhibitor of the K15P-PLCγ1 interaction, K15P-dependent PLCγ1 phosphorylation, NFAT-dependent promoter activation and the increased invasiveness and angiogenic properties of KSHV infected endothelial cells. We increased the binding of the PLCγ2 cSH2 domain for K15P by substituting two amino acids, thereby creating an improved dominant negative inhibitor of the K15P-dependent PLCγ1 activation. Taken together, these results demonstrate a necessary role of K15 in the increased invasiveness and angiogenesis of KSHV infected endothelial cells and suggest the K15-PLCγ1 interaction as a possible new target for inhibiting the angiogenic and invasive properties of KSHV.
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