ArticleJournal of virology2009
X-box binding protein 1 contributes to induction of the Kaposi's sarcoma-associated herpesvirus lytic cycle under hypoxic conditions.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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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.
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Who cites it
41 citing papers in PubMed, 58 citations in OpenAlex.
- Transcriptional factor ATF3 impairs KSHV lytic replication by suppressing the expression of viral bZIP protein K8.PLoS pathogens · 2026Article
- Stage-specific regulation of KSHV infection by HIF-1α.Journal of virology · 2026Article
- Inhibiting HSP27 activates the XBP1s/CerS1 interplay, which triggers DRP1-driven mitophagy, thereby protecting against cell death and promoting the KSHV lytic cycle in primary effusion lymphoma cells.Cell death discovery · 2026Article
- Viral cis-regulatory elements as sensors of cellular states and environmental cues.Trends in genetics : TIG · 2024Review
- Malignancy and viral infections in Sub-Saharan Africa: A review.Frontiers in virology (Lausanne, Switzerland) · 2023Article
- Single-cell analysis of Kaposi's sarcoma-associated herpesvirus infection in three-dimensional air-liquid interface culture model.PLoS pathogens · 2022Article
- Investigating the structural changes due to adenosine methylation of the Kaposi's sarcoma-associated herpes virus ORF50 transcript.PLoS computational biology · 2022Article
- Caspase-Mediated Cleavage of the Transcription Factor Sp3: Possible Relevance to Cancer and the Lytic Cycle of Kaposi's Sarcoma-Associated Herpesvirus.Microbiology spectrum · 2022Article
- The regulation of KSHV lytic reactivation by viral and cellular factors.Current opinion in virology · 2022Review
- Regulation of KSHV Latency and Lytic Reactivation.Viruses · 2020Review
- Sp3 Transcription Factor Cooperates with the Kaposi's Sarcoma-Associated Herpesvirus ORF50 Protein To Synergistically Activate Specific Viral and Cellular Gene Promoters.Journal of virology · 2020Article
- The RNA quality control pathway nonsense-mediated mRNA decay targets cellular and viral RNAs to restrict KSHV.Nature communications · 2020Article
- Gammaherpesviruses and B Cells: A Relationship That Lasts a Lifetime.Viral immunology · 2020Review
- Induction of Kaposi's Sarcoma-Associated Herpesvirus-Encoded Thymidine Kinase (ORF21) by X-Box Binding Protein 1.Journal of virology · 2020Article
- Herpesviruses and the Unfolded Protein Response.Viruses · 2019Review
- KSHV activates unfolded protein response sensors but suppresses downstream transcriptional responses to support lytic replication.PLoS pathogens · 2019Article
- A role of hypoxia-inducible factor 1 alpha in Murine Gammaherpesvirus 68 (MHV68) lytic replication and reactivation from latency.PLoS pathogens · 2019Article
- Nucleolar stress enhances lytic reactivation of the Kaposi's sarcoma-associated herpesvirus.Oncotarget · 2018Article
- Regulation of gammaherpesvirus lytic replication by endoplasmic reticulum stress-induced transcription factors ATF4 and CHOP.The Journal of biological chemistry · 2018Article
- Effects of the NEDD8-Activating Enzyme Inhibitor MLN4924 on Lytic Reactivation of Kaposi's Sarcoma-Associated Herpesvirus.Journal of virology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV), like other herpesviruses, has two stages to its life cycle: latency and lytic replication. KSHV is required for development of Kaposi's sarcoma, a tumor of endothelial origin, and is associated with the B-cell tumor primary effusion lymphoma (PEL) and the plasmablastic variant of multicentric Castleman's disease, all of which are characterized by predominantly latent KSHV infection. Recently, we and others have shown that the activated form of transcription factor X-box binding protein 1 (XBP-1) is a physiological trigger of KSHV lytic reactivation in PEL. Here, we show that XBP-1s transactivates the ORF50/RTA promoter though an ACGT core containing the XBP-1 response element, an element previously identified as a weakly active hypoxia response element (HRE). Hypoxia induces the KSHV lytic cycle, and active HREs that respond to hypoxia-inducible factor 1alpha are present in the ORF50/RTA promoter. Hypoxia also induces active XBP-1s, and here, we show that both transcription factors contribute to the induction of RTA expression, leading to the production of infectious KSHV under hypoxic conditions.
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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.