Inefficient establishment of KSHV latency suggests an additional role for continued lytic replication in Kaposi sarcoma pathogenesis
Author:
Publisher
American Society for Clinical Investigation
Subject
General Medicine
Reference71 articles.
1. The Biology of Kaposi’s Sarcoma
2. Molecular analysis of clonality in Kaposi's sarcoma.
3. Evidence for multiclonality in multicentric Kaposi's sarcoma
4. Monoclonality or Oligoclonality of Human Herpesvirus 8 Terminal Repeat Sequences in Kaposi's Sarcoma and Other Diseases
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1. Virus-induced paraspeckle-like condensates are essential hubs for gene expression and their formation drives genomic instability;2024-07-23
2. K v 1.3-induced hyperpolarization is required for efficient Kaposi’s sarcoma–associated herpesvirus lytic replication;Science Signaling;2024-07-16
3. KSHV vIL-6 promotes SIRT3-induced deacetylation of SERBP1 to inhibit ferroptosis and enhance cellular transformation by inducing lipoyltransferase 2 mRNA degradation;PLOS Pathogens;2024-03-12
4. RUNX3 inhibits KSHV lytic replication by binding to the viral genome and repressing transcription;Journal of Virology;2024-02-20
5. Kaposi's sarcoma herpesvirus exploits the DNA damage response to circularize its genome;Nucleic Acids Research;2024-01-05
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