Evidence map›Paper›PMID 17942556›Full record

ArticleJournal of virology2008

Inhibition of methyltransferases results in induction of g2/m checkpoint and programmed cell death in human T-lymphotropic virus type 1-transformed cells.

Arindam Dasgupta, Kyung-Jin Jung, Soo-Jin Jeong, John N Brady

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. HTLV-1 and apoptosis: role in cellular transformation and recent advances in therapeutic approaches.Apoptosis : an international journal on programmed cell death · 2008
    Review
  11. 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

4 authors at 3 institutions in 1 country.

Arindam DasguptaVirus Tumor Biology Section, Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 41 Medlars Dr., Building 41, Room B201, Bethesda, MD 20892, USA.
Kyung-Jin Jung
Soo-Jin Jeong
John N Brady
National Cancer Institute · USCenter for Cancer Research · USNational Institutes of Health · US

Funding

INTERACTION OF HTLV-I TAX WITH CELLULAR REGULATORY PROTEINSZ01BC005691 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BRADY, JOHN N. · 1996 to 2008
$2.3M
REGULATION OF VIRAL AND CELLULAR GENE EXPRESSONZ01BC005254 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BRADY, JOHN N. · 1996 to 2008
$1.1M
Inhibition of p53 Tumor Suppressor Function by HTLV-IZIABC005691 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BRADY, JOHN N. · 2009 to 2009
$709k
Regulation of HTLV-I TranscriptionZIABC005254 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BRADY, JOHN N. · 2009 to 2009
$532k
Intramural NIH HHS
6 · The paper itself

Abstract

Human T-lymphotropic virus type 1 (HTLV-1) is the etiologic agent for adult T-cell leukemia. The HTLV-1-encoded protein Tax transactivates the viral long terminal repeat and plays a critical role in virus replication and transformation. Previous work from our laboratory demonstrated that coactivator-associated arginine methytransferase 1, a protein arginine methytransferase, was important for Tax-mediated transactivation. To further investigate the role of methyltransferases in viral transcription, we utilized adenosine-2,3-dialdehyde (AdOx), an adenosine analog and S-adenosylmethionine-dependent methyltransferase inhibitor. The addition of AdOx decreased Tax transactivation in C81, Hut102, and MT-2 cells. Unexpectedly, we found that AdOx potently inhibited the growth of HTLV-1-transformed cells. Further investigation revealed that AdOx inhibited the Tax-activated NF-kappaB pathway, resulting in reactivation of p53 and induction of p53 target genes. Analysis of the NF-kappaB pathway demonstrated that AdOx treatment resulted in degradation of the IkappaB kinase complex and inhibition of NF-kappaB through stabilization of the NF-kappaB inhibitor IkappaBalpha. Our data further demonstrated that AdOx induced G(2)/M cell cycle arrest and cell death in HTLV-1-transformed but not control lymphocytes. These studies demonstrate that protein methylation plays an important role in NF-kappaB activation and survival of HTLV-1-transformed cells.

Indexed as

ApoptosisCell CycleCell LineCell ProliferationEnzyme InhibitorsGene Products, taxHumansHuman T-lymphotropic virus 1I-kappa B KinaseI-kappa B ProteinsMethyltransferasesNF-kappa BNF-KappaB Inhibitor alphaTumor Suppressor Protein p53Virus ReplicationEnzyme InhibitorsGene Products, taxI-kappa B KinaseI-kappa B ProteinsMethyltransferasesNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanTumor Suppressor Protein p53

Identifiers

PMID17942556
PMCPMC2224405
OpenAlexW2062663879

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.