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A structure-function analysis of transcriptional repression mediated by the WT1, Wilms' tumor suppressor protein.

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The chromosome 11p13 Wilms' tumor locus (wt1) encodes a zinc finger-containing transcription factor (WT1). WT1 binds to the consensus sequence (5'-GCGGGGGCG-3') and represses transcription when bound to this site in vivo. The mechanism of repression is not yet defined. To investigate the mechanisms

[Four new cases with WT1 gene mutations in Chinese patients with Wilms' tumor].

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OBJECTIVE Wilms' tumor (WT) is the most common malignant renal tumor in childhood. The WT1 gene located at 11p13 was identified in 1990 as a tumor suppressor gene important in the development in WT. The WT1 gene consists of 10 exons, with exons 1 to 6 encoding an N-terminal proline- and

Differentially spliced exon 5 of the Wilms' tumor gene WT1 modifies gene function.

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The Wilms' tumor gene WT1 encodes a zinc-finger transcription factor that functions as a tumor suppressor gene and repress transcription of a number of growth factors and proto-oncogenes. In the developing kidney, WT1 expression peaks at the onset of the mesenchyme-to-epithelium transition and is

RNA polymerase chain reaction detects different levels of four alternatively spliced WT1 transcripts in Wilms' tumors.

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A Wilms' tumor susceptibility gene (WT1) localized to 11p13 was recently isolated and shown to be altered in some sporadic Wilms' tumors. This gene encodes a DNA-binding protein with four zinc fingers (ZFs) in the carboxy-terminal region and a glutamine/proline (Gln/Pro)-rich domain near the 5' end.

TP53 codon 72 polymorphisms in favorable histology Wilms tumors.

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In Wilms tumor (WT), mutations in the gene encoding p53, TP53, are correlated with anaplasia; however TP53 variants have not been studied in favorable histology (FH) WTs. A single nucleotide polymorphism of TP53 encoding either arginine or proline at codon 72 is suggested to alter in vitro p53

Distinct functional properties of three human paired-box-protein, PAX8, isoforms generated by alternative splicing in thyroid, kidney and Wilms' tumors.

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The mammalian paired box (Pax) genes encode a family of transcription factors involved in embryogenesis. The murine and human Pax8 genes are expressed in developing and adult thyroid as well as in the developing secretory system and at the lower level in adult kidney. In the secretory system

cDNA cloning and its pronephros-specific expression of the Wilms' tumor suppressor gene, WT1, from Xenopus laevis.

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The Wilms' tumor suppressor gene, WT1, plays a crucial role during early urogenital development in mammals. To elucidate the function of WT1 in other vertebrates, we isolated the Xenopus WT1 homolog (XeWT1) from a testis cDNA library. Comparison of the XeWT1 protein with other WT1 proteins revealed

The WT1 Wilms tumor gene product: a developmentally regulated transcription factor in the kidney that functions as a tumor suppressor.

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Alteration of transcription factor function is becoming a common theme in molecular mechanisms of oncogenesis. A recent example of this trend is the isolation and characterization of the chromosome 11p13 Wilms tumor suppressor gene, WT1. The WT1 protein contains a DNA binding domain consisting of

Alternative splicing and genomic structure of the Wilms tumor gene WT1.

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The chromosome 11p13 Wilms tumor susceptibility gene WT1 appears to play a crucial role in regulating the proliferation and differentiation of nephroblasts and gonadal tissue. The WT1 gene consists of 10 exons, encoding a complex pattern of mRNA species: four distinct transcripts are expressed,

Transcriptional repression mediated by the WT1 Wilms tumor gene product.

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The wt1 gene, a putative tumor suppressor gene located at the Wilms tumor (WT) locus on chromosome 11p13, encodes a zinc finger-containing protein that binds to the same DNA sequence as EGR-1, a mitogen-inducible immediate-early gene product that activates transcription. The transcriptional

The Wilms' tumor gene product, WT1, represses transcription of the platelet-derived growth factor A-chain gene.

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The Wilms' tumor locus on chromosome 11p13 contains a tumor suppressor gene, wt1, which encodes a DNA binding protein (WT1) with four zinc fingers and a glutamine-proline-rich N terminus and which functions as a repressor of transcription. The platelet-derived growth factor (PDGF) A-chain gene

Transcriptional activation of the syndecan-1 promoter by the Wilms' tumor protein WT1.

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The Wilms' tumor suppressor gene (wt1) encodes a zinc finger DNA binding protein (WT1) which functions as a transcriptional regulator and is essential for normal urogenital development. WTI has previously been shown to repress the transcription of a variety of target genes whose products stimulate

Immunohistochemical expression of GLUT1 and its correlation with unfavorable histology and TP53 codon 72 polymorphism in Wilms tumors.

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Reprogramming of energy metabolism, such as increased glycolysis, is a hallmark of cancer cells. One mechanism by which cancer cells fuel glycolysis is through increased uptake of glucose across cell membranes via the glucose transporter GLUT1. One of the transcriptional repressors of GLUT1 is

Isolation and characterization of a zinc finger polypeptide gene at the human chromosome 11 Wilms' tumor locus.

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We have isolated a series of genomic and cDNA clones mapping within the boundaries of constitutional and tumor deletions that define the Wilms' tumor locus on human chromosome 11 (band p13). The transcription unit corresponding to these clones spans approximately 50 kb and encodes an mRNA

Characterization of the human forkhead gene FREAC-4. Evidence for regulation by Wilms' tumor suppressor gene (WT-1) and p53.

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We describe the cloning and sequence analysis of a nearly full-length cDNA as well as a corresponding 5.2-kilobase pair genomic fragment encoding FREAC-4, a member of the forkhead family of transcription factors. The cDNA is collinear with respect to the coding region of the intronless genomic

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