Evidence map›Paper›PMID 14766965›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2004

Identification of a human NF-kappaB-activating protein, TAB3.

Ge Jin, Alison Klika, Michelle Callahan, Ben Faga, Joel Danzig, Zhengfan Jiang, Xiaoxia Li, George R Stark, John Harrington, Bruce Sherf

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 81 citations in OpenAlex.

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  9. LncRNA PCIR Is an Oncogenic DriverFrontiers in oncology · 2021
    Article
  10. Apolipoprotein E Signals via TLR4 to Induce CXCL5 Secretion by Asthmatic Airway Epithelial Cells.American journal of respiratory cell and molecular biology · 2020
    Article
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  16. TAB3 overexpression promotes cell proliferation in non-small cell lung cancer and mediates chemoresistance to CDDP in A549 cells via the NF-κB pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

10 authors at 3 institutions in 1 country.

Ge JinAthersys, Inc., 3201 Carnegie Avenue, Cleveland, OH 44115, USA.
Alison Klika
Michelle Callahan
Ben Faga
Joel Danzig
Zhengfan Jiang
Xiaoxia Li
George R Stark
John Harrington
Bruce Sherf
Athersys (United States) · USCleveland Clinic · USCase Comprehensive Cancer Center

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NF-kappaB pathway plays a critical role in regulating cellular processes such as immune responses, stress responses, apoptosis, proliferation and differentiation, whereas dysfunction of this pathway has been associated with numerous cancer and immune disorders. We have applied our Random Activation of Gene Expression technology to an NF-kappaB reporter cell line to facilitate the discovery of positive regulators of NF-kappaB activation. A small protein expression library, corresponding to approximately 0.1x genome coverage, was generated and screened for clones exhibiting constitutive activation of NF-kappaB. After isolation of cellular clones displaying the relevant phenotypes, we identified two known components of the NF-kappaB pathway and a hypothetical gene that we have designated the human ortholog of Xenopus TAK1-binding protein 3 (TAB3). Overexpression of human TAB3 was found to activate both NF-kappaB and AP-1 transcription factors. Furthermore, the activation of NF-kappaB by TAB3 was blocked by the NF-kappaB inhibitor, SN50, and by expression of dominant-negative forms of tumor necrosis factor alpha-associated factor 6 and transforming growth factor beta-activated kinase. Taken together, these data demonstrate that TAB3 transforming growth factor is a constituent of the NF-kappaB pathway functioning upstream of tumor necrosis factor alpha-associated factor 6/transforming growth factor beta-activated kinase. Interestingly, increased expression of TAB3 was found in some cancer tissues, and its overexpression in NIH 3T3 cells resulted in cellular transformation, thus establishing a causative link between elevated TAB3 expression, constitutive NF-kappaB activation, and oncogenesis.

Indexed as

Adaptor Proteins, Signal TransducingIntracellular Signaling Peptides and ProteinsAmino Acid SequenceAnimalsCarrier ProteinsCell LineComputational BiologyElectrophoretic Mobility Shift AssayEnzyme-Linked Immunosorbent AssayGene Expression RegulationGenes, ReporterHumansInterleukin-8MAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMiceAdaptor Proteins, Signal TransducingCarrier ProteinsInterleukin-8Intracellular Signaling Peptides and ProteinsMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNF-kappa BPeptidesProteinsSN50 peptideTAB2 protein, humanTab2 protein, mouseTAB3 protein, humanTNF Receptor-Associated Factor 6

Identifiers

PMID14766965
PMCPMC357046
OpenAlexW2088633139

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.