Evidence map›Paper›PMID 21705495›Full record

ArticleBlood2011

HTLV-1 bZIP factor enhances TGF-β signaling through p300 coactivator.

Tiejun Zhao, Yorifumi Satou, Kenji Sugata, Paola Miyazato, Patrick L Green, Takeshi Imamura, Masao Matsuoka

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

84 citing papers in PubMed, 146 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. mGenes to cells : devoted to molecular & cellular mechanisms · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. JunB-HBZ nuclear translocation by TGF-β is a key driver in HTLV-1-mediated leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. IncreasedInternational journal of molecular sciences · 2024
    Article
  17. Vulnerability to APOBEC3G linked to the pathogenicity of deltaretroviruses.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Article
  19. Article
  20. Upregulation of Neuropilin-1 Inhibits HTLV-1 Infection.Pathogens (Basel, Switzerland) · 2023
    Article

24 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

7 authors at 3 institutions in 2 countries.

Tiejun ZhaoLaboratory of Virus Control, Institute for Virus Research, Kyoto University, Kyoto, Japan.
Yorifumi Satou
Kenji Sugata
Paola Miyazato
Patrick L Green
Takeshi Imamura
Masao Matsuoka
Kyoto University · JPJapanese Foundation For Cancer Research · JPThe Ohio State University · US

Funding

Role of Inflammation in Tax-mediated TumorigenesisP01CA100730 · NCI · WASHINGTON UNIVERSITY · PI Malachi Griffith · 2003 to 2026
$44.8M
ROLE OF HTLV TAX IN THE TRANSFORMATION OF HUMAN T CELLSR01CA077556 · NCI · OHIO STATE UNIVERSITY · PI GREEN, PATRICK LEE · 1997 to 2009
$1.8M
NCI NIH HHS CA100730NCI NIH HHS CA77556NCI NIH HHS P01 CA100730NCI NIH HHS R01 CA077556
6 · The paper itself

Abstract

Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus that is etiologically associated with adult T-cell leukemia. The HTLV-1 bZIP factor (HBZ), which is encoded by the minus strand of the provirus, is involved in both regulation of viral gene transcription and T-cell proliferation. We showed in this report that HBZ interacted with Smad2/3, and enhanced transforming growth factor-β (TGF-β)/Smad transcriptional responses in a p300-dependent manner. The N-terminal LXXLL motif of HBZ was responsible for HBZ-mediated TGF-β signaling activation. In a serial immunoprecipitation assay, HBZ, Smad3, and p300 formed a ternary complex, and the association between Smad3 and p300 was markedly enhanced in the presence of HBZ. In addition, HBZ could overcome the repression of the TGF-β response by Tax. Finally, HBZ expression resulted in enhanced transcription of Pdgfb, Sox4, Ctgf, Foxp3, Runx1, and Tsc22d1 genes and suppression of the Id2 gene; such effects were similar to those by TGF-β. In particular, HBZ induced Foxp3 expression in naive T cells through Smad3-dependent TGF-β signaling. Our results suggest that HBZ, by enhancing TGF-β signaling and Foxp3 expression, enables HTLV-1 to convert infected T cells into regulatory T cells, which is thought to be a critical strategy for virus persistence.

Indexed as

AnimalsBasic-Leucine Zipper Transcription FactorsCell LineCell Line, TumorE1A-Associated p300 ProteinForkhead Transcription FactorsGene Expression Regulation, LeukemicGene Expression Regulation, ViralHTLV-I InfectionsHumansHuman T-lymphotropic virus 1Leukemia-Lymphoma, Adult T-CellMiceMice, Inbred C57BLProtein Structure, TertiaryRetroviridae ProteinsBasic-Leucine Zipper Transcription FactorsE1A-Associated p300 ProteinEP300 protein, humanForkhead Transcription FactorsHBZ protein, human T-cell leukemia virus type IRetroviridae ProteinsSmad Proteins, Receptor-RegulatedTranscription Factor AP-1Transforming Growth Factor betaViral Proteins

Identifiers

PMID21705495
PMCPMC3158717
OpenAlexW2092834432

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.