Evidence map›Paper›PMID 16155604›Full record

ReviewOncogene2005

Molecular mechanisms of cellular transformation by HTLV-1 Tax.

Ralph Grassmann, Mordechai Aboud, Kuan-Teh Jeang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
218citing papers in PubMed, 1 pooled it
9.4field-weighted citation impact, top 1% 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

218 citing papers in PubMed, 1 synthesis or guideline pooled it, 378 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Cancer Microbiology.Journal of the National Cancer Institute · 2022
    Article
  17. Therapeutic potentials of CRISPR-Cas genome editing technology in human viral infections.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022
    Review
  18. Review
  19. Article
  20. A role for an HTLV-1 vaccine?Frontiers in immunology · 2022
    Review

158 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

3 authors at 3 institutions in 3 countries.

Ralph GrassmannInstitut für Klinische und Molekulare Virologie, Universität Erlangen-Nürnberg, Schlossgarten 4, Germany. Ralph.Grassmann@viro.med.uni-erlangen.de
Mordechai Aboud
Kuan-Teh Jeang
Ben-Gurion University of the Negev · ILFriedrich-Alexander-Universität Erlangen-Nürnberg · DENational Institute of Allergy and Infectious Diseases · US

Funding

Molecular Mechanisms Of Human Immunodeficiency Virus Trans-regulatory ProteinsZIAAI000547 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI JEANG, KUAN-TEH · 2009 to 2013
$5.9M
MOLECULAR MECHANISMS OF HUMAN RETROVIRUS TRANS-REGULATORY PROTEINSZ01AI000547 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI JEANG, KUAN-TEH · 1989 to 2008
$2.8M
6 · The paper itself

Abstract

The HTLV Tax protein is crucial for viral replication and for initiating malignant transformation leading to the development of adult T-cell leukemia. Tax has been shown to be oncogenic, since it transforms and immortalizes rodent fibroblasts and human T-lymphocytes. Through CREB, NF-kappaB and SRF pathways Tax transactivates cellular promoters including those of cytokines (IL-13, IL-15), cytokine receptors (IL-2Ralpha) and costimulatory surface receptors (OX40/OX40L) leading to upregulated protein expression and activated signaling cascades (e.g. Jak/STAT, PI3Kinase, JNK). Tax also stimulates cell growth by direct binding to cyclin-dependent kinase holenzymes and/or inactivating tumor suppressors (e.g. p53, DLG). Moreover, Tax silences cellular checkpoints, which guard against DNA structural damage and chromosomal missegregation, thereby favoring the manifestation of a mutator phenotype in cells.

Indexed as

Cell Transformation, NeoplasticAnimalsCytokinesDNA DamageGene Products, taxHumansHuman T-lymphotropic virus 1MutationPromoter Regions, GeneticReceptors, Cell SurfaceSignal TransductionT-LymphocytesTranscriptional ActivationVirus ReplicationCytokinesGene Products, taxReceptors, Cell Surface

Identifiers

PMID16155604
OpenAlexW2079929369

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.