Evidence map›Paper›PMID 15560845›Full record

ArticleRetrovirology2004

Human T lymphotropic virus type-1 p30II alters cellular gene expression to selectively enhance signaling pathways that activate T lymphocytes.

Bindhu Michael, Amrithraj M Nair, Hajime Hiraragi, Lei Shen, Gerold Feuer, Kathleen Boris-Lawrie, Michael D Lairmore

Open access · goldAbstract read
In one paragraph

Article in Retrovirology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.5field-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

33 citing papers in PubMed, 41 citations in OpenAlex.

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  20. HTLV-1 and apoptosis: role in cellular transformation and recent advances in therapeutic approaches.Apoptosis : an international journal on programmed cell death · 2008
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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 4 institutions in 1 country.

Bindhu MichaelCenter for Retrovirus Research, Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio 43210, USA. bindhu_michael@merck.com
Amrithraj M Nair
Hajime Hiraragi
Lei Shen
Gerold Feuer
Kathleen Boris-Lawrie
Michael D Lairmore
The Ohio State University · USThe Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · USSUNY Upstate Medical University · USUnited States Military Academy · US

Funding

Role of Inflammation in Tax-mediated TumorigenesisP01CA100730 · NCI · WASHINGTON UNIVERSITY · PI Malachi Griffith · 2003 to 2026
$44.8M
ANIMAL MODELS OF MOLECULAR PATHOGENSIS OF HTLV-1R01RR014324 · NCRR · OHIO STATE UNIVERSITY · PI LAIRMORE, MICHAEL D · 1999 to 2003
$1.2M
NCI NIH HHS CA100730NCI NIH HHS CA-70529NCI NIH HHS P01 CA100730NCRR NIH HHS R01 RR014324NCRR NIH HHS RR14324
6 · The paper itself

Abstract

backgroundHuman T-lymphotropic virus type-1 (HTLV-1) is a deltaretrovirus that causes adult T-cell leukemia/lymphoma and is implicated in a variety of lymphocyte-mediated disorders. HTLV-1 contains both regulatory and accessory genes in four pX open reading frames. pX ORF-II encodes two proteins, p13II and p30II, which are incompletely defined in the virus life cycle or HTLV-1 pathogenesis. Proviral clones of the virus with pX ORF-II mutations diminish the ability of the virus to maintain viral loads in vivo. Exogenous expression of p30II differentially modulates CREB and Tax-responsive element-mediated transcription through its interaction with CREB-binding protein/p300 and represses tax/rex RNA nuclear export.

resultsHerein, we further characterized the role of p30II in regulation of cellular gene expression, using stable p30II expression system employing lentiviral vectors to test cellular gene expression with Affymetrix U133A arrays, representing approximately 33,000 human genes. Reporter assays in Jurkat T cells and RT-PCR in Jurkat and primary CD4+ T-lymphocytes were used to confirm selected gene expression patterns. Our data reveals alterations of interrelated pathways of cell proliferation, T-cell signaling, apoptosis and cell cycle in p30II expressing Jurkat T cells. In all categories, p30II appeared to be an overall repressor of cellular gene expression, while selectively increasing the expression of certain key regulatory genes.

conclusionsWe are the first to demonstrate that p30II, while repressing the expression of many genes, selectively activates key gene pathways involved in T-cell signaling/activation. Collectively, our data suggests that this complex retrovirus, associated with lymphoproliferative diseases, relies upon accessory gene products to modify cellular environment to promote clonal expansion of the virus genome and thus maintain proviral loads in vivo.

Indexed as

Gene Expression RegulationApoptosisHumansHuman T-lymphotropic virus 1Jurkat CellsLymphocyte ActivationNF-kappa BOpen Reading FramesSignal TransductionT-LymphocytesTranscription, GeneticNF-kappa B

Identifiers

PMID15560845
PMCPMC538277
OpenAlexW2149776653

What OpenQuestion holds

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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.