Evidence map›Paper›PMID 18511807›Full record

ArticleBlood2008

Central role of PI3K in transcriptional activation of hTERT in HTLV-I-infected cells.

Marcia Bellon, Christophe Nicot

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
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  4. TheCells · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Marcia BellonDepartment of Microbiology, Immunology, and Molecular Genetics, University of Kansas Medical Center, Kansas City, USA.
Christophe Nicot
University of Kansas Medical Center · US

Funding

Mechanisms of human T-cell immortalization by HTLV-I TaxR01CA106258 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI NICOT, CHRISTOPHE P · 2005 to 2015
$2.2M
Uncoupling of Jak/STAT in HTLV-1 associated leukemiaR01CA115398 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI NICOT, CHRISTOPHE P · 2007 to 2011
$1.3M
NCI NIH HHS CA106258NCI NIH HHS CA115398NCI NIH HHS R01 CA106258NCI NIH HHS R01 CA115398
6 · The paper itself

Abstract

The persistence of human T-cell leukemia/lymphoma virus-I (HTLV-I)-infected cells is dependent upon clonal expansion and up-regulation of telomerase (hTERT). We have previously found that in interleukin (IL)-2-independent transformed HTLV-I cells, Tax strongly activates the hTERT promoter through nuclear factor-kappaB (NF-kappaB)-mediated Sp1 and c-Myc activation. In IL-2-dependent cells and adult T-cell leukemia/lymphoma (ATLL) patient samples, however, Tax expression is very low to undetectable, yet these cells retain strong telomerase activity. This suggests the existence of compensatory mechanisms in IL-2-dependent cells and ATLL patients. In this study, we demonstrate that telomerase activity is significantly decreased upon IL-2 withdrawal in immortalized HTLV-I cell lines. Inhibition of PI3K or AKT signaling pathways reduced telomerase activity in HTLV-I cells. We found that IL-2/IL-2R signaling was associated with a PI3K-dependent/AKT-independent transcriptional up-regulation of the endogenous hTERT promoter. We found that activation of the PI3K pathway mediated cytoplasmic retention of the Wilms tumor (WTI) protein, which strongly suppressed the hTERT promoter. The importance of this regulatory pathway for telomerase expression is underscored by findings that the PI3K pathway is commonly found activated in cancer cells.

Indexed as

Cell LineCell Line, TransformedCell Transformation, NeoplasticEnzyme ActivationHTLV-I InfectionsHumansHuman T-lymphotropic virus 1Interleukin-2Phosphatidylinositol 3-KinasesPromoter Regions, GeneticProtein BindingProto-Oncogene Proteins c-aktReceptors, Interleukin-2Signal TransductionTelomeraseTranscriptional ActivationInterleukin-2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Interleukin-2TelomeraseTERT protein, humanWT1 Proteins

Identifiers

PMID18511807
PMCPMC2556626
OpenAlexW1973985923

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.