ArticleVirology2007
Transcriptional repression of K-Rta by Kaposi's sarcoma-associated herpesvirus K-bZIP is not required for oriLyt-dependent DNA replication.
Article in Virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Degradation of TRIM32 is induced by RTA for Kaposi's sarcoma-associated herpesvirus lytic replication.Journal of virology · 2024Article
- Viral manipulation of the cellular sumoylation machinery.Cell communication and signaling : CCS · 2017Review
- KSHV Genome Replication and Maintenance.Frontiers in microbiology · 2016Review
- The Modulation of Apoptotic Pathways by Gammaherpesviruses.Frontiers in microbiology · 2016Review
- Molecular biology of KSHV lytic reactivation.Viruses · 2015Review
- Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus Latency and Reactivation.Advances in virology · 2011Article
- Kaposi sarcoma-associated herpesvirus (KSHV): molecular biology and oncogenesis.Cancer letters · 2010Review
- Initiation of lytic DNA replication in Epstein-Barr virus: search for a common family mechanism.Future virology · 2010Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Kaposi's sarcoma-associated herpesvirus origin-dependent DNA replication requires the core replication proteins plus K-Rta and K-bZIP. To determine which K-bZIP protein domains contribute to oriLyt-dependent DNA replication and facilitate suppression of K-Rta-mediated transcriptional activation, we generated a series of deletion constructs and site-directed mutations within the K-bZIP ORF. Mutation of key leucine residues within the putative leucine zipper (LZ) motif eliminated the ability of the protein to homodimerize and complement oriLyt-dependent DNA replication. Deletion of the basic amino acid region (BR) or LZ domain did not affect the ability of K-bZIP to bind to K-Rta indicating that either region contributes to heterodimerization with K-Rta. However, deletions or mutations introduced into both the LZ and BR resulted in elimination of the suppressive activity of K-bZIP even in the presence of a K-bZIP-K-Rta interaction. Interestingly, mutants that lacked the ability to suppress K-Rta transactivation were still capable of complementing oriLyt-dependent DNA replication, indicating that this activity does not contribute to the DNA synthesis-related activity of K-bZIP.
Indexed as
Identifiers
What OpenQuestion holds
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.