ArticleMolecular and cellular biology1997
Concerted activity of host cell factor subregions in promoting stable VP16 complex assembly and preventing interference by the acidic activation domain.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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Who cites it
34 citing papers in PubMed, 48 citations in OpenAlex.
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- Duck Plague Virus pUL48 Protein Activates the Immediate-Early Gene to Initiate the Transcription of the Virus Gene.Frontiers in microbiology · 2021Article
- ICP22/IE63 Mediated Transcriptional Regulation and Immune Evasion: Two Important Survival Strategies for Alphaherpesviruses.Frontiers in immunology · 2021Review
- The Role of VP16 in the Life Cycle of Alphaherpesviruses.Frontiers in microbiology · 2020Review
- Characteristics of herpes simplex virus infection and pathogenesis suggest a strategy for vaccine development.Reviews in medical virology · 2019Review
- HCF-2 inhibits cell proliferation and activates differentiation-gene expression programs.Nucleic acids research · 2019Article
- The mutated tegument protein UL7 attenuates the virulence of herpes simplex virus 1 by reducing the modulation of α-4 gene transcription.Virology journal · 2016Article
- HSV-1 tegument protein and the development of its genome editing technology.Virology journal · 2016Review
- HCF-1 self-association via an interdigitated Fn3 structure facilitates transcriptional regulatory complex formation.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Krox20 controls the transcription of its various targets in the developing hindbrain according to multiple modes.The Journal of biological chemistry · 2009Article
- Cellular and viral factors regulate the varicella-zoster virus gE promoter during viral replication.Journal of virology · 2007Article
- HCF-1 functions as a coactivator for the zinc finger protein Krox20.The Journal of biological chemistry · 2003Article
- Proteolytic processing is necessary to separate and ensure proper cell growth and cytokinesis functions of HCF-1.The EMBO journal · 2003Article
- Human Sin3 deacetylase and trithorax-related Set1/Ash2 histone H3-K4 methyltransferase are tethered together selectively by the cell-proliferation factor HCF-1.Genes & development · 2003Article
- Molecular cloning of Drosophila HCF reveals proteolytic processing and self-association of the encoded protein.Journal of cellular physiology · 2003Article
- Interaction of HCF-1 with a cellular nuclear export factor.The Journal of biological chemistry · 2002Article
- An activation domain in the C-terminal subunit of HCF-1 is important for transactivation by VP16 and LZIP.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Inactivation of the retinoblastoma protein family can bypass the HCF-1 defect in tsBN67 cell proliferation and cytokinesis.Molecular and cellular biology · 2002Article
- Stabilization but not the transcriptional activity of herpes simplex virus VP16-induced complexes is evolutionarily conserved among HCF family members.Journal of virology · 2001Article
- DNA recognition by the herpes simplex virus transactivator VP16: a novel DNA-binding structure.Molecular and cellular biology · 2001Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In contrast to our understanding of the roles of Oct-1 and VP16 in VP16-mediated transcriptional activation, virtually nothing is known of the role of the second cellular component, termed host cell factor (HCF), or of its structure-function relationships. We show that the majority of the internal region of HCF, including the repeats involved in HCF cleavage, is dispensable for complex assembly with VP16 and Oct-1. The N-terminal domain of HCF (HCF.N) had only weak VP16 binding and complex promoting activity, while the C-terminal region (HCF.C) had no intrinsic activity. However, the C-terminal region strongly enhanced complex formation and reduced dissociation kinetics when linked to the N-terminal domain (HCF.NC). The potent activity of the HCF.NC fusion in complex assembly was recapitulated in vivo in yeast and mammalian cells. Moreover, HCF.N could promote increased complex formation when the acidic activation domain of VP16 was deleted. Restoration of the activation domain strongly inhibited complex formation with HCF.N, but the addition of the C-terminal domain of HCF restored strong stable complex formation with intact VP16. The results indicate that this C-terminal domain is critically required to alter the presentation of the acidic domain of VP16. Additional results are consistent with the interpretation that this alteration in acidic domain presentation for complex assembly also facilitates the activation function in VP16. The sequence of an HCF homolog from Caenorhabditis elegans shows it to be a natural HCF.NC construct, reinforcing the conclusions from our functional analysis.
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