KSHV reactivation from latency requires Pim-1 and Pim-3 kinases to inactivate the latency-associated nuclear antigen LANA.
Host signal-transduction pathways are intimately involved in the switch between latency and productive infection of herpes viruses. As with other herpes viruses, infection by Kaposi's sarcoma herpesvirus (KSHV) displays these two phases. During latency only few viral genes are expressed, while...
Guardado en:
Autores principales: | Fang Cheng, Magdalena Weidner-Glunde, Markku Varjosalo, Eeva-Marja Rainio, Anne Lehtonen, Thomas F Schulz, Päivi J Koskinen, Jussi Taipale, Päivi M Ojala |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
Public Library of Science (PLoS)
2009
|
Materias: | |
Acceso en línea: | https://doaj.org/article/9cccbbca394040a6aa99a96faf1f7381 |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
Ejemplares similares
-
Nucleophosmin phosphorylation by v-cyclin-CDK6 controls KSHV latency.
por: Grzegorz Sarek, et al.
Publicado: (2010) -
Latently KSHV-Infected Cells Promote Further Establishment of Latency upon Superinfection with KSHV
por: Chen Gam ze Letova, et al.
Publicado: (2021) -
Influence of ND10 components on epigenetic determinants of early KSHV latency establishment.
por: Thomas Günther, et al.
Publicado: (2014) -
PIM kinases mediate resistance to cisplatin chemotherapy in hepatoblastoma
por: Raoud Marayati, et al.
Publicado: (2021) -
Hierarchical control on polyene macrolide biosynthesis: PimR modulates pimaricin production via the PAS-LuxR transcriptional activator PimM.
por: Javier Santos-Aberturas, et al.
Publicado: (2012)