ArticleBlood2006
KSHV G protein-coupled receptor inhibits lytic gene transcription in primary-effusion lymphoma cells via p21-mediated inhibition of Cdk2.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 46 citations in OpenAlex.
- Association of NFκB and related-cytokines with the viral load and development of antibodies against HHV-8 in people living with HIV/AIDS.Medical microbiology and immunology · 2020Article
- Metabolic reprogramming of Kaposi's sarcoma associated herpes virus infected B-cells in hypoxia.PLoS pathogens · 2018Article
- Herpesvirus-encoded GPCRs: neglected players in inflammatory and proliferative diseases?Nature reviews. Drug discovery · 2014Review
- KSHV: pathways to tumorigenesis and persistent infection.Advances in virus research · 2014Review
- KSHV Rta Promoter Specification and Viral Reactivation.Frontiers in microbiology · 2012Article
- Oxidative stress induces reactivation of Kaposi's sarcoma-associated herpesvirus and death of primary effusion lymphoma cells.Journal of virology · 2011Article
- NF-κB as a target for oncogenic viruses.Current topics in microbiology and immunology · 2011Review
- Cell membrane-bound Kaposi's sarcoma-associated herpesvirus-encoded glycoprotein B promotes virus latency by regulating expression of cellular Egr-1.The Journal of biological chemistry · 2010Article
- Convergence of Kaposi's sarcoma-associated herpesvirus reactivation with Epstein-Barr virus latency and cellular growth mediated by the notch signaling pathway in coinfected cells.Journal of virology · 2010Article
- The role of macrophages in the development and progression of AIDS-related non-Hodgkin lymphoma.Journal of leukocyte biology · 2010Review
- The phosphatase Shp2 is required for signaling by the Kaposi's sarcoma-associated herpesvirus viral GPCR in primary endothelial cells.Virology · 2010Article
- Role of ORF74-encoded viral G protein-coupled receptor in human herpesvirus 8 lytic replication.Journal of virology · 2009Article
- Article
- NF-kappaB p50 plays distinct roles in the establishment and control of murine gammaherpesvirus 68 latency.Journal of virology · 2009Article
- Activation of host translational control pathways by a viral developmental switch.PLoS pathogens · 2009Article
- Regulation of the retinoblastoma proteins by the human herpesviruses.Cell division · 2009Article
- Identification of direct transcriptional targets of the Kaposi's sarcoma-associated herpesvirus Rta lytic switch protein by conditional nuclear localization.Journal of virology · 2008Article
- Desensitization of herpesvirus-encoded G protein-coupled receptors.Life sciences · 2008Review
- Article
- Targeted therapy for Kaposi's sarcoma and Kaposi's sarcoma-associated herpesvirus.Current opinion in oncology · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Kaposi sarcoma (KS) remains the most common AIDS-associated malignancy worldwide. In sub-Saharan Africa especially, this aggressive endothelial-cell tumor is a cause of widespread morbidity and mortality. Infection with Kaposi sarcoma-associated herpesvirus (KSHV) is now known to be an etiologic force behind KS and primary-effusion lymphoma (PEL). Over time, KSHV has pirated many human genes whose products regulate angiogenesis, inflammation, and the cell cycle. One of these, the KSHV vGPCR, is a lytic product that is a constitutively active homolog of the IL-8 receptor. Although it is considered a viral oncogene and causes KS-like lesions in mice, vGPCR expression results in cell-cycle arrest of KSHV-infected PEL cells. In the present study, we show that this arrest is mediated by p21 in a p53-independent manner; the resulting Cdk2 inhibition decreases the efficiency of chemical induction of KSHV lytic transcripts ORF 50 and 26. Importantly, Cdk2 activity is also essential for replication in other human herpesviruses. The ability of vGPCR to delay or abort KSHV replication may explain how despite being a lytic product, this potent signaling molecule has a vital role in tumor formation via its induction of various KS-associated cytokines.
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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.