ArticleJournal of virology2008
Association of the cellular coactivator HCF-1 with the Golgi apparatus in sensory neurons.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- The opportunities and challenges of epigenetic approaches to manage herpes simplex infections.Expert review of anti-infective therapy · 2024Review
- Models of Herpes Simplex Virus Latency.Viruses · 2024Review
- Key questions on the epigenetics of herpes simplex virus latency.PLoS pathogens · 2022Article
- Regulation of host and virus genes by neuronal miR-138 favours herpes simplex virus 1 latency.Nature microbiology · 2021Article
- [Mechanisms of herpes simplex virus latency and reactivation].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2019Review
- CREB3 Transcription Factors: ER-Golgi Stress Transducers as Hubs for Cellular Homeostasis.Frontiers in cell and developmental biology · 2019Review
- Herpes Simplex Virus Establishment, Maintenance, and Reactivation: In Vitro Modeling of Latency.Pathogens (Basel, Switzerland) · 2017Review
- Article
- Cloning and characterization of rat Luman/CREB3, a transcription factor highly expressed in nervous system tissue.Journal of molecular neuroscience : MN · 2015Article
- A neuron-specific host microRNA targets herpes simplex virus-1 ICP0 expression and promotes latency.Cell host & microbe · 2014Article
- Complexity of Interferon-γ Interactions with HSV-1.Frontiers in immunology · 2014Review
- The dynamics of HCF-1 modulation of herpes simplex virus chromatin during initiation of infection.Viruses · 2013Review
- Targeting the JMJD2 histone demethylases to epigenetically control herpesvirus infection and reactivation from latency.Science translational medicine · 2013Article
- The molecular basis of herpes simplex virus latency.FEMS microbiology reviews · 2012Review
- Entry of herpes simplex virus type 1 (HSV-1) into the distal axons of trigeminal neurons favors the onset of nonproductive, silent infection.PLoS pathogens · 2012Article
- Article
- EBV tegument protein BNRF1 disrupts DAXX-ATRX to activate viral early gene transcription.PLoS pathogens · 2011Article
- Tegument protein control of latent herpesvirus establishment and animation.Herpesviridae · 2011Article
- Transcriptional coactivator HCF-1 couples the histone chaperone Asf1b to HSV-1 DNA replication components.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Inhibition of the histone demethylase LSD1 blocks alpha-herpesvirus lytic replication and reactivation from latency.Nature medicine · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
HCF-1 is a cellular transcriptional coactivator that is critical for mediating the regulated expression of the immediate-early genes of the alphaherpesviruses herpes simplex virus type 1 and varicella-zoster virus. HCF-1 functions, at least in part, by modulating the modification of nucleosomes at these viral promoters to reverse cell-mediated repressive marks and promote activating marks. Strikingly, HCF-1 is specifically sequestered in the cytoplasm of sensory neurons where these viruses establish latency and is rapidly relocalized to the nucleus upon stimuli that result in viral reactivation. However, the analysis of HCF-1 in latently infected neurons and the protein's specific subcellular location have not been determined. Therefore, in this study, the localization of HCF-1 in unstimulated and induced latently infected sensory neurons was investigated and was found to be similar to that observed in uninfected mice, with a time course of induced nuclear accumulation that correlated with viral reactivation. Using a primary neuronal cell culture system, HCF-1 was localized to the Golgi apparatus in unstimulated neurons, a unique location for a transcriptional coactivator. Upon disruption of the Golgi body, HCF-1 was rapidly relocalized to the nucleus in contrast to other Golgi apparatus-associated proteins. The location of HCF-1 is distinct from that of CREB3, an endoplasmic reticulum-resident HCF-1 interaction partner that has been proposed to sequester HCF-1. The results support the model that HCF-1 is an important component of the viral latency-reactivation cycle and that it is regulated by association with a component that is distinct from the identified HCF-1 interaction factors.
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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.