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Functional interaction between class II histone deacetylases and ICP0 of herpes simplex virus type 1Detection of the genome and transcripts of a persistent DNA virus in neuronal tissues by fluorescent in situ hybridization combined with immunostaining.HSV-1 genome subnuclear positioning and associations with host-cell PML-NBs and centromeres regulate LAT locus transcription during latency in neurons.Centromere architecture breakdown induced by the viral E3 ubiquitin ligase ICP0 protein of herpes simplex virus type 1.Centromeric protein CENP-B proteasomal degradation induced by the viral protein ICP0.Establishment of HSV1 latency in immunodeficient mice facilitates efficient in vivo reactivation.The interaction between herpes simplex virus 1 genome and promyelocytic leukemia nuclear bodies (PML-NBs) as a hallmark of the entry in latency.Real-Time Tracking of Parental Histones Reveals Their Contribution to Chromatin Integrity Following DNA Damage.Herpesvirus Latency: On the Importance of Positioning Oneself.Characterization of antiproliferative and cytotoxic properties of the HSV-1 immediate-early ICPo protein.Bovine herpesvirus 4: genomic organization and relationship with two other gammaherpesviruses, Epstein-Barr virus and herpesvirus saimiri.Expression of the epidermodysplasia verruciformis-associated genes EVER1 and EVER2 is activated by exogenous DNA and inhibited by LMP1 oncoprotein from Epstein-Barr virusBiological features of herpes simplex virus type 1 latency in mice according to experimental conditions and type of neurones.The protein ICP0 of herpes simplex virus type 1 is targeted to nucleoli of infected cells. Brief report.Promyelocytic leukemia (PML) nuclear bodies (NBs) induce latent/quiescent HSV-1 genomes chromatinization through a PML NB/Histone H3.3/H3.3 Chaperone Axis
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description
researcher
@en
name
P Lomonte
@en
P Lomonte
@nl
type
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P Lomonte
@en
P Lomonte
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prefLabel
P Lomonte
@en
P Lomonte
@nl
P106
P31
P496
0000-0001-9248-648X