Evidence map›Paper›PMID 18078517›Full record

ArticleRetrovirology2007

HTLV-1 HBZ cooperates with JunD to enhance transcription of the human telomerase reverse transcriptase gene (hTERT).

Anne-Sophie Kuhlmann, Julien Villaudy, Louis Gazzolo, Marc Castellazzi, Jean-Michel Mesnard, Madeleine Duc Dodon

Open access · goldAbstract read
In one paragraph

Article in Retrovirology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

79 citing papers in PubMed, 127 citations in OpenAlex.

  1. Assessing the validity of leucine zipper constructs predicted by AlphaFold.Protein science : a publication of the Protein Society · 2026
    Article
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  3. Upregulation of Neuropilin-1 Inhibits HTLV-1 Infection.Pathogens (Basel, Switzerland) · 2023
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19 more citing papers are in PubMed but not listed here.

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

6 authors at 5 institutions in 1 country.

Anne-Sophie KuhlmannVirologie Humaine, INSERM-U758, 69364 Lyon Cedex 07, France. anne-sophie.kuhlmann@ens-lyon.fr
Julien Villaudy
Louis Gazzolo
Marc Castellazzi
Jean-Michel Mesnard
Madeleine Duc Dodon
Inserm · FRCentre National de la Recherche Scientifique · FRÉcole Normale Supérieure de Lyon · FRInstitut Français de l'Éducation · FRVirologie et Pathologies Humaines · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundActivation of telomerase is a critical and late event in tumor progression. Thus, in patients with adult-T cell leukaemia (ATL), an HTLV-1 (Human T cell Leukaemia virus type 1)-associated disease, leukemic cells display a high telomerase activity, mainly through transcriptional up-regulation of the human telomerase catalytic subunit (hTERT). The HBZ (HTLV-1 bZIP) protein coded by the minus strand of HTLV-1 genome and expressed in ATL cells has been shown to increase the transcriptional activity of JunD, an AP-1 protein. The presence of several AP-1 binding sites in the hTERT promoter led us to investigate whether HBZ regulates hTERT gene transcription.

resultsHere, we demonstrate using co-transfection assays that HBZ in association with JunD activates the hTERT promoter. Interestingly, the -378/+1 proximal region, which does not contain any AP-1 site was found to be responsible for this activation. Furthermore, an increase of hTERT transcripts was observed in cells co-expressing HBZ and JunD. Chromatin immunoprecipitation (ChIP) assays revealed that HBZ, and JunD coexist in the same DNA-protein complex at the proximal region of hTERT promoter. Finally, we provide evidence that HBZ/JunD heterodimers interact with Sp1 transcription factors and that activation of hTERT transcription by these heterodimers is mediated through GC-rich binding sites for Sp1 present in the proximal sequences of the hTERT promoter.

conclusionThese observations establish for the first time that HBZ by intervening in the re-activation of telomerase, may contribute to the development and maintenance of the leukemic process.

Indexed as

Transcription, GeneticUp-RegulationBasic-Leucine Zipper Transcription FactorsChromatin ImmunoprecipitationDimerizationDNAHumansHuman T-lymphotropic virus 1Promoter Regions, GeneticProtein BindingProto-Oncogene Proteins c-junRetroviridae ProteinsRNA, MessengerSp1 Transcription FactorTelomeraseViral ProteinsBasic-Leucine Zipper Transcription FactorsDNAHBZ protein, human T-cell leukemia virus type IProto-Oncogene Proteins c-junRetroviridae ProteinsRNA, MessengerSp1 Transcription FactorTelomeraseTERT protein, humanViral Proteins

Identifiers

PMID18078517
PMCPMC2235888
OpenAlexW2153277134

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.