Evidence map›Paper›PMID 19709433›Full record

ArticleMolecular cancer2009

STAT5 regulation of BCL10 parallels constitutive NFkappaB activation in lymphoid tumor cells.

Zsuzsanna S Nagy, Matthew J LeBaron, Jeremy A Ross, Abhisek Mitra, Hallgeir Rui, Robert A Kirken

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. LGMNFrontiers in immunology · 2026
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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

6 authors at 3 institutions in 1 country.

Zsuzsanna S NagyDepartment of Biological Sciences, University of Texas at El Paso, El Paso, TX 79968, USA. znagy@utep.edu
Matthew J LeBaron
Jeremy A Ross
Abhisek Mitra
Hallgeir Rui
Robert A Kirken
The University of Texas at El Paso · USDow Chemical (United States) · USThomas Jefferson University · US

Funding

TOXICOLOGY PROJECTG12RR008124 · NCRR · UNIVERSITY OF TEXAS EL PASO · PI WALSH, ELIZABETH J · 1992 to 2011
$20.8M
UTEP SCORE InstrumentationS06GM008012 · NIGMS · UNIVERSITY OF TEXAS EL PASO · PI GARZA, KRISTINE M · 1989 to 2010
$15.8M
NCRR NIH HHS 5G12RR008124NCRR NIH HHS G12 RR008124NIGMS NIH HHS S06 GM008012NIGMS NIH HHS S06 GM008012-37
6 · The paper itself

Abstract

backgroundSignal Transducer and Activator of Transcription 5 A and B (STAT5) are key survival factors in cells of the lymphoid lineage. Identification of novel, tissue-specific STAT5 regulated genes would advance the ability to combat diseases due to aberrant STAT5 signaling. In the present work a library of human STAT5 bound genomic elements was created and validated.

resultsOf several STAT5 responsive genomic regulatory elements identified, one was located within the first intron of the human BCL10 gene. Chromatin immuno-precipitation reactions confirmed constitutive in vivo STAT5 binding to this intronic fragment in various human lymphoid tumor cell lines. Interestingly, non-phosphorylated STAT5 was found in the nuclei of Kit225 and YT cells in the absence of cytokine stimulation that paralleled constitutive NFkappaB activation. Inhibition of the hyperactive JAK3/STAT5 pathway in MT-2 cells via the Mannich-base, NC1153, diminished the constitutive in vivo occupancy of BCL10-SBR by STAT5, reduced NFkappaB activity and BCL10 protein expression in a dose dependent manner. Moreover, depletion of STAT5 via selective antisense oligonucleotide treatment similarly resulted in decreased BCL10 mRNA and protein expression, cellular viability and impaired NFkappaB activity independent of IL-2.

conclusionThese results suggest that the NFkappaB regulator BCL10 is an IL-2-independent STAT5 target gene. These findings proffer a model in which un-activated STAT5 can regulate pathways critical for lymphoid cell survival and inhibitors that disrupt STAT5 function independent of tyrosine phosphorylation may be therapeutically effective in treating certain leukemias/lymphomas.

Indexed as

Gene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingB-Cell CLL-Lymphoma 10 ProteinBinding SitesBlotting, WesternCell LineCell Line, TumorCell SurvivalChromatin ImmunoprecipitationDose-Response Relationship, DrugElectrophoretic Mobility Shift AssayGenomic LibraryHumansInterleukin-2Janus Kinase 3LymphomaAdaptor Proteins, Signal TransducingB-Cell CLL-Lymphoma 10 ProteinBCL10 protein, humanInterleukin-2JAK3 protein, humanJanus Kinase 3Mannich BasesNC 1153NF-kappa BOligodeoxyribonucleotides, AntisenseSTAT5 Transcription Factor

Identifiers

PMID19709433
PMCPMC2741462
OpenAlexW2168680029

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.