ArticleVirology2010
The phosphatase Shp2 is required for signaling by the Kaposi's sarcoma-associated herpesvirus viral GPCR in primary endothelial cells.
Article in Virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Cancers associated with human gammaherpesviruses.The FEBS journal · 2022Review
- Protein Tyrosine Phosphatase SHP2 Suppresses Host Innate Immunity against Influenza A Virus by Regulating EGFR-Mediated Signaling.Journal of virology · 2021Article
- Modulation of oncogenic signaling networks by Kaposi's sarcoma-associated herpesvirus.Biological chemistry · 2017Review
- Mutations in the C-terminal region affect subcellular localization of crucian carp herpesvirus (CaHV) GPCR.Virus genes · 2016Article
- Identification of Th1/Th2 regulatory switch to promote healing response during leishmaniasis: a computational approach.EURASIP journal on bioinformatics & systems biology · 2015Article
- SHP-2 Mediates Cryptosporidium parvum Infectivity in Human Intestinal Epithelial Cells.PloS one · 2015Article
- The regulatory roles of phosphatases in cancer.Oncogene · 2014Review
- Latent KSHV infection of endothelial cells induces integrin beta3 to activate angiogenic phenotypes.PLoS pathogens · 2011Article
- The Kaposi's sarcoma-associated herpesvirus G protein-coupled receptor contains an immunoreceptor tyrosine-based inhibitory motif that activates Shp2.Journal of virology · 2011Article
- Modulation of chemokine activity by viruses.Current opinion in immunology · 2010Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi's sarcoma (KS), an AIDS-related endothelial cell malignancy that is the most common cancer in central and southern Africa. The KSHV viral G protein-coupled receptor (vGPCR) is a viral oncogene that conveys a survival advantage to endothelial cells and causes KS-like tumors in mouse models. In this study we investigate the role of Shp2, a protein tyrosine phosphatase in vGPCR signaling. Shp2 is vital to many cytokine-induced signaling pathways and is dysregulated in various infections and malignancies. It has also recently been implicated in angiogenesis. We find that vGPCR activity results in phosphorylation of regulatory tyrosines in Shp2 and that in turn, Shp2 is required for vGPCR-mediated activation of MEK, NFkappaB, and AP-1. Furthermore, both genetic and chemical inhibition of Shp2 abrogate vGPCR-induced enhancement of endothelial cell migration. This establishes Shp2 as an important point of convergence of KSHV vGPCR signaling and a potential molecular target in the design of an anti-KSHV therapeutic regimen.
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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.