Evidence map›Paper›PMID 9553050›Full record

ArticleGenes & development1998

pX, the HBV-encoded coactivator, suppresses the phenotypes of TBP and TAFII250 mutants.

I Haviv, Y Matza, Y Shaul

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed, 31 citations in OpenAlex.

  1. Structural and biochemical analysis of Bcl-2 interaction with the hepatitis B virus protein HBx.Proceedings of the National Academy of Sciences of the United States of America · 2016
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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

3 authors at 1 institution in 1 country.

I HavivDepartment of Molecular Genetics, The Weizmann Institute of Science, Rehovot 76100 Israel.
Y Matza
Y Shaul
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) infects humans and causes a wide range of clinical manifestations, from acute hepatitis to hepatocellular carcinoma (HCC). The HBV genome contains multiple promoters with gene expression regulated predominantly by the cellular transcription initiation machinery. Accordingly, the HBV-encoded pX, the only known viral regulator, is a potent transcription coactivator. We investigated the relationship between pX and cellular coactivators. We show that pX restores wild-type activity to inactive TBPAS mutants with poor TAFII250 and activator-binding activity. This pX-mediated recovery, however, is not obtained with inactive TBPAS mutants in binding of other general transcription factors. Remarkably, ts13, a cell line temperature sensitive for TAFII250 function, exhibiting growth arrest and apoptosis at the restrictive temperature, is rescued partially by pX expression, thus generating a pX-dependent cell growth. Collectively, our results suggest that pX suppresses some of the phenotypes of TBP and TAFII250 mutations, implying that pX circumvents the need for a holo-TFIID complex for transcription activation to proceed.

Indexed as

MutagenesisTATA-Binding Protein Associated FactorsTranscription Factor TFIIDAnimalsCell CycleCell LineCOS CellsCricetinaeCyclin ADNA-Binding ProteinsGene Expression RegulationHepatitis B AntigensHepatitis B virusHistone AcetyltransferasesHumansNuclear ProteinsCyclin ADNA-Binding ProteinsHepatitis B Antigenshepatitis B virus X proteinHistone AcetyltransferasesNuclear ProteinsTATA-binding protein associated factor 250 kDaTATA-Binding Protein Associated FactorsTATA-Box Binding ProteinTrans-ActivatorsTranscription FactorsTranscription Factor TFIIDViral Regulatory and Accessory Proteins

Identifiers

PMID9553050
PMCPMC316710
OpenAlexW2057547110

What OpenQuestion holds

Textmetadata
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Registered trials

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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.