ArticleBritish journal of cancer1998
Wilms' tumour-suppressor protein isoforms have opposite effects on Igf2 expression in primary embryonic cells, independently of p53 genotype.
Article in British journal of cancer, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Genotype-Phenotype Correlations in Denys-Drash Syndrome in Children.Kidney international reports · 2025Article
- Human IGF2 Gene Epigenetic and Transcriptional Regulation: At the Core of Developmental Growth and Tumorigenic Behavior.Biomedicines · 2023Review
- Distinct global binding patterns of the Wilms tumor gene 1 (WT1) -KTS and +KTS isoforms in leukemic cells.Haematologica · 2017Article
- Mechanisms of transcriptional regulation by WT1 (Wilms' tumour 1).The Biochemical journal · 2014Review
- Different isoforms of the Wilms' tumour protein WT1 have distinct patterns of distribution and trafficking within the nucleus.Cell proliferation · 2006Article
- EGR-1 enhances tumor growth and modulates the effect of the Wilms' tumor 1 gene products on tumorigenicity.Oncogene · 2000Article
- The Wilms' tumor gene product represses the transcription of thrombospondin 1 in response to overexpression of c-Jun.Oncogene · 1999Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
The p53 protein has been proposed as a modulator of the Wilms' tumour-suppressor protein (WT1) transcriptional regulation activity. To investigate this putative p53 role, the promoter P3 of the mouse insulin-like growth factor II gene (Igf2) was used as a target for WT1 regulation in primary cell cultures derived from p53 wild-type (p53+/+) and knock-out (p53-/-) mouse embryos. In these cells, the WT1 transcriptional activity was observed to be independent of p53 genotype. Furthermore, the two WT1 zinc finger (ZF) isoforms were for the first time found to have opposite effects on gene expression from a single promoter in the same cell type, WT1[-KTS] activating Igf2 P3, whereas WT1[+KTS] repressed its activity. In addition, we have mapped the WT1 binding sites and investigated the effect on WT1 binding activity of individual ZF deletions and Denys-Drash syndrome point mutations to this target.
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