Evidence map›Paper›PMID 26804169›Full record

ArticleOncogene2016

HTLV-1 bZIP factor protein targets the Rb/E2F-1 pathway to promote proliferation and apoptosis of primary CD4(+) T cells.

A Kawatsuki, J-I Yasunaga, Y Mitobe, P L Green, M Matsuoka

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. The Pleiotropic Effects of YBX1 on HTLV-1 Transcription.International journal of molecular sciences · 2023
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Bioinformatic-based mechanism identification ofJournal of gastrointestinal oncology · 2022
    Article
  11. Article
  12. Role of Virus-Induced Host Cell Epigenetic Changes in Cancer.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Article
  15. Review
  16. HTLV-1 induces T cell malignancy and inflammation by viral antisense factor-mediated modulation of the cytokine signaling.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Article
  18. Review
  19. Review
  20. Article
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

5 authors at 2 institutions in 2 countries.

A KawatsukiLaboratory of Virus Control, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto, Japan.
J-I YasunagaLaboratory of Virus Control, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto, Japan.
Y MitobeLaboratory of Virus Control, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto, Japan.
P L GreenCenter for Retrovirus Research and Departments of Veterinary Biosciences and Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, OH, USA.
M MatsuokaLaboratory of Virus Control, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto, Japan.ORCID 0000-0002-0473-754X
Kyoto University · JPThe Ohio State University · US

Funding

Role of Inflammation in Tax-mediated TumorigenesisP01CA100730 · NCI · WASHINGTON UNIVERSITY · PI Malachi Griffith · 2003 to 2026
$44.8M
NCI NIH HHS P01 CA100730
6 · The paper itself

Abstract

Human T-cell leukemia virus type 1 (HTLV-1) is an oncogenic retrovirus that induces a fatal T-cell malignancy, adult T-cell leukemia (ATL). Among several regulatory/accessory genes in HTLV-1, HTLV-1 bZIP factor (HBZ) is the only viral gene constitutively expressed in infected cells. Our previous study showed that HBZ functions in two different molecular forms, HBZ protein and HBZ RNA. In this study, we show that HBZ protein targets retinoblastoma protein (Rb), which is a critical tumor suppressor in many types of cancers. HBZ protein interacts with the Rb/E2F-1 complex and activates the transcription of E2F-target genes associated with cell cycle progression and apoptosis. Mouse primary CD4(+) T cells transduced with HBZ show accelerated G1/S transition and apoptosis, and importantly, T cells from HBZ transgenic (HBZ-Tg) mice also demonstrate enhanced cell proliferation and apoptosis. To evaluate the functions of HBZ protein alone in vivo, we generated a new transgenic mouse strain that expresses HBZ mRNA altered by silent mutations but encoding intact protein. In these mice, the numbers of effector/memory and Foxp3(+) T cells were increased, and genes associated with proliferation and apoptosis were upregulated. This study shows that HBZ protein promotes cell proliferation and apoptosis in primary CD4(+) T cells through activation of the Rb/E2F pathway, and that HBZ protein also confers onto CD4(+) T-cell immunophenotype similar to those of ATL cells, suggesting that HBZ protein has important roles in dysregulation of CD4(+) T cells infected with HTLV-1.

Indexed as

ApoptosisAnimalsBasic-Leucine Zipper Transcription FactorsCD4-Positive T-LymphocytesCell CycleCell ProliferationCells, CulturedE2F1 Transcription FactorHistone Deacetylase 3Histone DeacetylasesHumansMiceMice, Inbred C57BLRetinoblastoma ProteinRetroviridae ProteinsSignal TransductionBasic-Leucine Zipper Transcription FactorsE2F1 protein, humanE2F1 Transcription FactorHBZ protein, human T-cell leukemia virus type IHistone Deacetylase 3Histone DeacetylasesRetinoblastoma ProteinRetroviridae ProteinsTumor Suppressor Protein p53

Identifiers

PMID26804169
PMCPMC4959989
OpenAlexW2256898151

What OpenQuestion holds

Textmetadata
LicenceTDM
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.