Evidence map›Paper›PMID 25341660›Full record

ReviewViruses2014

Regulation of HTLV-1 tax stability, cellular trafficking and NF-κB activation by the ubiquitin-proteasome pathway.

Alfonso Lavorgna, Edward William Harhaj

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
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  6. Article
  7. Review
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  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Molecular mechanisms of viral oncogenesis in humans.Nature reviews. Microbiology · 2018
    Review
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

2 authors at 2 institutions in 1 country.

Alfonso LavorgnaDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA. alavorg1@jhmi.edu.
Edward William HarhajDepartment of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, Baltimore, MD 21287, USA. eharhaj1@jhmi.edu.
Johns Hopkins University · USSidney Kimmel Comprehensive Cancer Center · US

Funding

Mechanisms of HTLV-I Tax-mediated NF-kB activationR01CA135362 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HARHAJ, EDWARD W · 2009 to 2018
$2.7M
NCI NIH HHS R01 CA135362NCI NIH HHS R01CA135362
6 · The paper itself

Abstract

Human T-cell leukemia virus type 1 (HTLV-1) is a complex retrovirus that infects CD4+ T cells and causes adult T-cell leukemia/lymphoma (ATLL) in 3%-5% of infected individuals after a long latent period. HTLV-1 Tax is a trans-activating protein that regulates viral gene expression and also modulates cellular signaling pathways to enhance T-cell proliferation and cell survival. The Tax oncoprotein promotes T-cell transformation, in part via constitutive activation of the NF-κB transcription factor; however, the underlying mechanisms remain unknown. Ubiquitination is a type of post-translational modification that occurs in a three-step enzymatic cascade mediated by E1, E2 and E3 enzymes and regulates protein stability as well as signal transduction, protein trafficking and the DNA damage response. Emerging studies indicate that Tax hijacks the ubiquitin machinery to activate ubiquitin-dependent kinases and downstream NF-κB signaling. Tax interacts with the E2 conjugating enzyme Ubc13 and is conjugated on C-terminal lysine residues with lysine 63-linked polyubiquitin chains. Tax K63-linked polyubiquitination may serve as a platform for signaling complexes since this modification is critical for interactions with NEMO and IKK. In addition to NF-κB signaling, mono- and polyubiquitination of Tax also regulate its subcellular trafficking and stability. Here, we review recent advances in the diverse roles of ubiquitin in Tax function and how Tax usurps the ubiquitin-proteasome pathway to promote oncogenesis.

Indexed as

Protein Processing, Post-TranslationalCarcinogenesisCell LineGene Expression RegulationGene Products, taxHumansHuman T-lymphotropic virus 1Leukemia-Lymphoma, Adult T-CellNF-kappa BProteasome Endopeptidase ComplexProtein TransportSignal TransductionUbiquitinUbiquitinationGene Products, taxNF-kappa BProteasome Endopeptidase Complextax protein, Human T-lymphotrophic virus 1Ubiquitin

Identifiers

PMID25341660
PMCPMC4213571
OpenAlexW1970748259

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.