Evidence map›Paper›PMID 10629049›Full record

ArticleMolecular and cellular biology2000

Mutations in host cell factor 1 separate its role in cell proliferation from recruitment of VP16 and LZIP.

S S Mahajan, A C Wilson

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Uncovering cancer dependencies in peptide-interacting protein pockets.bioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Article
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  5. Article
  6. Sequence variants in host cell factor C1 are associated with Ménière's disease.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2008
    Article
  7. Article
  8. Site-specific proteolysis of the transcriptional coactivator HCF-1 can regulate its interaction with protein cofactors.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. N-terminal transcriptional activation domain of LZIP comprises two LxxLL motifs and the host cell factor-1 binding motif.Proceedings of the National Academy of Sciences of the United States of America · 2000
    Article
  14. Article
  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

S S MahajanDepartment of Microbiology, Kaplan Comprehensive Cancer Center, New York University School of Medicine, New York, New York 10016, USA.
A C Wilson
New York University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Host cell factor 1 (HCF-1) is a nuclear protein required for progression through G(1) phase of the cell cycle and, via its association with VP16, transcriptional activation of the herpes simplex virus immediate-early genes. Both functions require a six-bladed beta-propeller domain encoded by residues 1 to 380 of HCF-1 as well as an additional amino-terminal region. The beta-propeller domain is well conserved in HCF homologues, consistent with a critical cellular function. To date, the only known cellular target of the beta-propeller is a bZIP transcription factor known as LZIP or Luman. Whether the interaction between HCF-1 and LZIP is required for cell proliferation remains to be determined. In this study, we used directed mutations to show that all six blades of the HCF-1 beta-propeller contribute to VP16-induced complex assembly, association with LZIP, and cell cycle progression. Although LZIP and VP16 share a common tetrapeptide HCF-binding motif, our results reveal profound differences in their interaction with HCF-1. Importantly, with several of the mutants we observe a poor correlation between the ability to associate with LZIP and promote cell proliferation in the context of the full HCF-1 amino terminus, arguing that the HCF-1 beta-propeller domain must target other cellular transcription factors in order to contribute to G(1) progression.

Indexed as

Amino Acid SequenceAmino Acid SubstitutionCell CycleCell DivisionCell LineCyclic AMP Response Element-Binding ProteinG1 PhaseHerpes Simplex Virus Protein Vmw65Host Cell Factor C1HumansLeucine ZippersMolecular Sequence DataMutagenesis, Site-DirectedProteinsProtein Structure, SecondaryRecombinant ProteinsCREB3 protein, humanCyclic AMP Response Element-Binding ProteinHCFC1 protein, humanHerpes Simplex Virus Protein Vmw65Host Cell Factor C1ProteinsRecombinant ProteinsTranscription Factors

Identifiers

PMID10629049
PMCPMC85209
OpenAlexW2141167234

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.