ArticleThe Journal of biological chemistry2012
Leucine zipper domain is required for Kaposi sarcoma-associated herpesvirus (KSHV) K-bZIP protein to interact with histone deacetylase and is important for KSHV replication.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 23 citations in OpenAlex.
- Exploitation of CREB signaling by HTLV-1 and BLV: A central axis in viral persistence and leukemogenesis.Medical oncology (Northwood, London, England) · 2026Review
- Genetic Conservation and Diversity of SARS-CoV-2 Envelope Gene Across Variants of Concern.Journal of medical virology · 2025Article
- Investigation of key miRNAs and Target-mRNA in Kaposi's sarcoma using bioinformatic methods.Heliyon · 2024Article
- Article
- Genome-Wide CRISPR-Cas9 Screen Identifies SMCHD1 as a Restriction Factor for Herpesviruses.mBio · 2023Article
- Marek's disease virus US3 protein kinase phosphorylates chicken HDAC 1 and 2 and regulates viral replication and pathogenesis.PLoS pathogens · 2021Article
- Marek's disease virus Meq oncoprotein interacts with chicken HDAC 1 and 2 and mediates their degradation via proteasome dependent pathway.Scientific reports · 2021Article
- Proteomic approaches to investigate gammaherpesvirus biology and associated tumorigenesis.Advances in virus research · 2021Review
- Regulation of KSHV Latency and Lytic Reactivation.Viruses · 2020Review
- The bZIP Proteins of Oncogenic Viruses.Viruses · 2020Review
- Towards Better Understanding of KSHV Life Cycle: from Transcription and Posttranscriptional Regulations to Pathogenesis.Virologica Sinica · 2019Review
- Sirtuin 6 Attenuates Kaposi's Sarcoma-Associated Herpesvirus Reactivation by Suppressing Ori-Lyt Activity and Expression of RTA.Journal of virology · 2019Article
- STAT6 degradation and ubiquitylated TRIML2 are essential for activation of human oncogenic herpesvirus.PLoS pathogens · 2018Article
- Viral manipulation of the cellular sumoylation machinery.Cell communication and signaling : CCS · 2017Review
- K-bZIP Mediated SUMO-2/3 Specific Modification on the KSHV Genome Negatively Regulates Lytic Gene Expression and Viral Reactivation.PLoS pathogens · 2015Article
- Recent advances in the study of Kaposi's sarcoma-associated herpesvirus replication and pathogenesis.Virologica Sinica · 2015Review
- Molecular biology of KSHV lytic reactivation.Viruses · 2015Review
- Primary macrophages rely on histone deacetylase 1 and 2 expression to induce type I interferon in response to gammaherpesvirus infection.Journal of virology · 2014Article
- Targeting sphingosine kinase induces apoptosis and tumor regression for KSHV-associated primary effusion lymphoma.Molecular cancer therapeutics · 2014Article
- A conserved gammaherpesvirus protein kinase targets histone deacetylases 1 and 2 to facilitate viral replication in primary macrophages.Journal of virology · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The Kaposi sarcoma-associated herpesvirus (KSHV; or human herpesvirus-8)-encoded protein called K-bZIP (also named K8) was found to be multifunctional. In this study, we discovered that K-bZIP interacts with histone deacetylase (HDAC) 1/2 in 12-O-tetradecanoylphorbol-13-acetate-stimulated BCBL-1 lymphocyte cells. K-bZIP appears to repress HDAC activity through this interaction, which we determined to be independent of K-bZIP SUMOylation. We dissected the domains of K-bZIP and found that the leucine zipper (LZ) domain is essential for the interaction of K-bZIP and HDAC. In addition, we constructed a KSHV bacterial artificial chromosome (BAC) with LZ domain-deleted K-bZIP (KSHVdLZ) and transfected this mutated KSHV BAC DNA into HEK 293T cells. As a result, it was consistently found that K-bZIP without its LZ domain failed to interact with HDAC2. We also showed that the interaction between K-bZIP and HDAC is necessary for the inhibition of the lytic gene promoters (ORF50 and OriLyt) of KSHV by K-bZIP. Furthermore, we found that the LZ domain is also important for the interaction of K-bZIP with the promoters of ORF50 and OriLyt. Most interestingly, although it was found to have suppressive effects on the promoters of ORF50 and OriLyt, KSHVdLZ replicates at a significantly lower level than its BAC-derived revertant (KSHVdLZRev) or KSHVWT (BAC36) in HEK 293T cells. The defectiveness of KSHVdLZ replication can be partially rescued by siRNA against HDAC2. Our results suggest that the function of K-bZIP interaction with HDAC is two-layered. 1) K-bZIP inhibits HDAC activity generally so that KSHVdLZ replicates at a lower level than does KSHVWT. 2) K-bZIP can recruit HDAC to the promoters of OriLyt and ORF50 through interaction with HDAC for K-bZIP to have a temporary repressive effect on the two promoters.
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