Evidence map›Paper›PMID 11243407›Full record

ArticleGene expression2000

The role of NF-kappaB in the regulation of the expression of wilms tumor suppressor gene WT1.

Y Chen, B R Williams

Open access · greenAbstract read
In one paragraph

Article in Gene expression, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 81% 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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
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

2 authors at 1 institution in 1 country.

Y ChenDepartment of Cancer Biology, Lerner Research Institute, Cleveland Clinic Foundation, OH 44195, USA.
B R Williams
Cleveland Clinic · US

Funding

FUNCTION OF WILMS TUMOR GENES IN NEPHROGENESISR01DK047101 · NIDDK · CLEVELAND CLINIC FOUNDATION · PI WILLIAMS, BRYAN R. G. · 1994 to 1997
–
NIDDK NIH HHS DK47101
6 · The paper itself

Abstract

The Wilms tumor suppressor gene, WT1, plays an important role in genitourinary development and the etiology of Wilms tumor. WT1 has a spatially and temporally defined expression in the developing genitourinary system and in specific cells of the hematopoietic system, but the regulatory pathways that control WT1 expression are not well understood. Recently, members of the NF-kappaB family of transcription factors have been proposed as potent activators of the murine WT1 promoter through binding to a NF-kappaB site. Because the human WT1 promoter contains a conserved NF-kappaB site, we investigated whether NF-kappaB also regulates the expression of the human WT1 gene. We activated NF-kappaB through cytokine stimulation or inhibited NF-kappaB through expression of a NF-kappaB "super repressor" in WT1 expressing Wilms tumor, renal carcinoma, and erythroleukemia cultures and examined the level of endogenous WT1 gene expression. Although a transfected NF-kappaB reporter construct was responsive to these manipulations, we found that altering NF-kappaB activity had no effect on endogenous WT1 expression in the cell types used in our study. We conclude that despite the presence of conserved NF-kappaB elements in the murine and human WT1 promoters, NF-kappaB is not required to regulate the expression of the WT1 gene in its natural context.

Indexed as

AnimalsBase SequenceDNA-Binding ProteinsDNA PrimersGene Expression RegulationGenes, Wilms TumorHumansMiceNF-kappa BPromoter Regions, GeneticTranscription FactorsTumor Cells, CulturedWilms TumorWT1 ProteinsDNA-Binding ProteinsDNA PrimersNF-kappa BTranscription FactorsWT1 Proteins

Identifiers

PMID11243407
PMCPMC5964932
OpenAlexW2406428950

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.