ArticleJournal of virology2003
Kaposi's sarcoma-associated herpesvirus latency-associated nuclear antigen induces expression of the helix-loop-helix protein Id-1 in human endothelial cells.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
- Review
- Single-cell analysis of Kaposi's sarcoma-associated herpesvirus infection in three-dimensional air-liquid interface culture model.PLoS pathogens · 2022Article
- Kaposi's sarcoma-associated herpesvirus infection promotes proliferation of SH-SY5Y cells by the Notch signaling pathway.Cancer cell international · 2021Article
- The Lymphatic Cell Environment Promotes Kaposi Sarcoma Development by Prox1-Enhanced Productive Lytic Replication of Kaposi Sarcoma Herpes Virus.Cancer research · 2020Article
- Kaposi's Sarcoma-Associated Herpesvirus LANA Modulates the Stability of the E3 Ubiquitin Ligase RLIM.Journal of virology · 2020Article
- Activation of DNA Damage Response Induced by the Kaposi's Sarcoma-Associated Herpes Virus.International journal of molecular sciences · 2016Review
- Cell Cycle Regulatory Functions of the KSHV Oncoprotein LANA.Frontiers in microbiology · 2016Review
- The Kaposi Sarcoma Herpesvirus Latency-associated Nuclear Antigen DNA Binding Domain Dorsal Positive Electrostatic Patch Facilitates DNA Replication and Episome Persistence.The Journal of biological chemistry · 2015Article
- Kaposi's Sarcoma-Associated Herpesvirus (KSHV) Induces the Oncogenic miR-17-92 Cluster and Down-Regulates TGF-β Signaling.PLoS pathogens · 2015Article
- KSHV LANA--the master regulator of KSHV latency.Viruses · 2014Review
- LANA binds to multiple active viral and cellular promoters and associates with the H3K4methyltransferase hSET1 complex.PLoS pathogens · 2014Article
- Oncogenic herpesvirus KSHV Hijacks BMP-Smad1-Id signaling to promote tumorigenesis.PLoS pathogens · 2014Article
- Article
- A protein array screen for Kaposi's sarcoma-associated herpesvirus LANA interactors links LANA to TIP60, PP2A activity, and telomere shortening.Journal of virology · 2012Article
- Phosphorylation of the chromatin binding domain of KSHV LANA.PLoS pathogens · 2012Article
- Kaposi's sarcoma herpesvirus upregulates Aurora A expression to promote p53 phosphorylation and ubiquitylation.PLoS pathogens · 2012Article
- The latency-associated nuclear antigen, a multifunctional protein central to Kaposi's sarcoma-associated herpesvirus latency.Future microbiology · 2011Review
- Human herpesvirus 8-associated neoplasms: the roles of viral replication and antiviral treatment.Current opinion in infectious diseases · 2011Review
- The single RBP-Jkappa site within the LANA promoter is crucial for establishing Kaposi's sarcoma-associated herpesvirus latency during primary infection.Journal of virology · 2011Article
- Pathology of Kaposi's Sarcoma-Associated Herpesvirus Infection.Frontiers in microbiology · 2011Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) (also known as human herpesvirus 8) is a gamma-2 herpesvirus believed to be the etiologic agent responsible for KS. The pathogenesis of this potentially life-threatening neoplasm is complex and unclear, and it is currently unknown how KSHV causes KS. Id (named for inhibitor of DNA binding or inhibitor of differentiation) proteins were identified in 1990 and found to be naturally occurring dominant-negative inhibitors of basic helix-loop-helix transcription factors. Id-1, the most well-studied member of this family, has since been shown to play a key role in several biological systems including cellular differentiation, cell cycle regulation, and tumorigenesis. In this report, we demonstrate that Id-1 is expressed at high levels in KS tumor cells both in vitro and in vivo but is expressed at relatively modest levels in endothelial cells (ECs), the likely precursor of the KS tumor cell. Infection of precursor cells with KSHV may be responsible for this enhanced expression, as KSHV infection induced Id-1 27-fold in ECs under our experimental conditions. Furthermore, we demonstrate that the KSHV-encoded latency-associated nuclear antigen (LANA) protein appears to be involved. Expression of LANA in ECs resulted in Id-1 induction that was almost identical to the induction seen with KSHV-infected ECs. These results demonstrate the expression of Id-1 in KS tumor cells and indicate the KSHV LANA protein may be, at least in part, responsible. This may be an important mechanism by which KSHV allows KS tumor cells to escape normal cell cycle regulation and enhances their proliferation.
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