Sequence of the WT1 Upstream Region Including the Wit-1 Gene

Gessler, Manfred; Bruns, G. A. P.

doi:10.1006/geno.1993.1355

Cited by 20 publications

(13 citation statements)

References 9 publications

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“…Internal sequencing and comparison with genomic sequences (NCBI build 36) showed that in each expressed transcript, exons were flanked by canonical splice donor and acceptor sites (GT-AG rule), indicating that these mRNAs represented bona fide spliced RNAs. Of the clones that we isolated from a fetal kidney cDNA library, AS1 and AS8 contained the major splice identified by Gessler and Bruns (1993), whereas clone AS9 had a novel splicing pattern that has not been described previously. Analysis of the complete cDNA sequences showed multiple small ORFs within these clones, the largest being 92 amino acids for AS1 (as described by Campbell et al 1994).…”

Section: Multiple Alternate Splicing Of Wt1-asmentioning

confidence: 60%

“…1). Screening of a human fetal kidney cDNA library identified two different classes of spliced cDNA, the first class of which (AS1/AS8-type) has been previously described (Gessler and Bruns 1993;Malik et al 2000), but the cDNAs described here extend the known 59 and 39 termini of this spliceoform substantially. The second class of cDNA (AS9) isolated from fetal kidney represents an entirely new spliceoform lacking the 1-kb intron that is present in AS1 and AS8, being spliced further 39 across a small (110 bp) and larger intron (7381 bp) before terminating in a 376-bp exon located 10 kbp upstream of the WT1 transcriptional start.…”

Section: Structure Of the Wt1 Antisense Transcript In Human And Mousementioning

confidence: 70%

“…A human fetal kidney l cDNA library (Clontech) was screened using a radiolabeled probe corresponding to the WIT-1 cDNA (Gessler and Bruns 1993), according to the manufacturers' protocols. Positive clones were identified on duplicate plates and the complete DNA sequence was obtained by automated sequencing (University of Durham).…”

Section: Library Screeningmentioning

confidence: 99%

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Alternately spliced WT1 antisense transcripts interact with WT1 sense RNA and show epigenetic and splicing defects in cancer

Dallosso¹,

Hancock²,

Malik³

et al. 2007

RNA

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Many mammalian genes contain overlapping antisense RNAs, but the functions and mechanisms of action of these transcripts are mostly unknown. WT1 is a well-characterized developmental gene that is mutated in Wilms' tumor (WT) and acute myeloid leukaemia (AML) and has an antisense transcript (WT1-AS), which we have previously found to regulate WT1 protein levels. In this study, we show that WT1-AS is present in multiple spliceoforms that are usually expressed in parallel with WT1 RNA in human and mouse tissues. We demonstrate that the expression of WT1-AS correlates with methylation of the antisense regulatory region (ARR) in WT1 intron 1, displaying imprinted monoallelic expression in normal kidney and loss of imprinting in WT. However, we find no evidence for imprinting of mouse Wt1-as. WT1-AS transcripts are exported into the cytoplasm and form heteroduplexes with WT1 mRNA in the overlapping region in WT1 exon 1. In AML, there is often abnormal splicing of WT1-AS, which may play a role in the development of this malignancy. These results show that WT1 encodes conserved antisense RNAs that may have an important regulatory role in WT1 expression via RNA:RNA interactions, and which can become deregulated by a variety of mechanisms in cancer.

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Section: Multiple Alternate Splicing Of Wt1-asmentioning

confidence: 60%

Section: Structure Of the Wt1 Antisense Transcript In Human And Mousementioning

confidence: 70%

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Alternately spliced WT1 antisense transcripts interact with WT1 sense RNA and show epigenetic and splicing defects in cancer

Dallosso¹,

Hancock²,

Malik³

et al. 2007

RNA

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“…We found that WIT-1 (Wilms' Tumor Upstream Neighbour 1) gene expression was most highly correlated to that of WT1 (partial correlation 0.244) which can be explained by shared promoter area (30). Besides WIT-1, QPRT was the gene whose transcription showed the highest correlation with that of WT1 (partial correlation 0.087).…”

Section: Expression Of Wt1 and Qprt Is Highly Correlated In Amlmentioning

confidence: 86%

Anti-apoptotic quinolinate phosphoribosyltransferase ( QPRT ) is a target gene of Wilms' tumor gene 1 (WT1) protein in leukemic cells

Ullmark

Montano

Järvstråt

et al. 2017

Biochemical and Biophysical Research Communications

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“…Alternative splicing of exon 5, or of nine base pairs within exon 9 which encode lysine, threonine and serine (KTS), generates four WT1 protein isoforms exhibiting dierent DNA-binding speci®cities Bickmore et al, 1992). The human WT1 promoter is G ± C rich, lacks a TATA box or CCAAT motif, and has multiple WT1 and SP1 binding sites (Hofmann et al, 1993;Campbell et al, 1994;Fraizer et al, 1994;Rupprecht et al, 1994;Gessler and Bruns, 1993). WT1 has been shown to negatively autoregulate its own expression (Rupprecht et al, 1994;Malik et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Differential regulation of the human Wilms tumour suppressor gene (WT1) promoter by two isoforms of PAX2

et al. 1997

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PAX2 is a member of the paired box family of genes with an important role in kidney, genital tract and eye development. Another gene essential for kidney and genital tract development is the Wilms tumour gene, WT1. PAX2 and WT1 encode transcription factors expressed during fetal kidney development in patterns that overlap both spatially and temporally. The overlap of PAX2 and WT1 expression in fetal kidney prompted us to determine whether PAX2 regulates the WT1 gene. To investigate this possibility, the WT1 promoter and a series of WT1 promoter deletion fragments were cloned into a luciferase reporter vector, and used in cotransfection experiments with PAX2 expression constructs. PAX2 transactivated the WT1 promoter up to 35-fold in CHO-K1 cells, and from four-to sevenfold in 293 cells. Two regions of the WT1 promoter were required in the same promoter construct for ecient transactivation by PAX2 in CHO-K1 cells, and puri®ed recombinant PAX2 protein was found to bind to two sites in the WT1 promoter, at 7205/7230 and +377/ +402. Removal of WT1 promoter sequences containing the 7205/7230, or +377/+402 binding sites abolished transactivation of the WT1 promoter by PAX2 in CHO-K1 cells, and had a dierential eect on transactivation of the WT1 promoter in 293 cells, depending on the PAX2 isoform used. A fragment containing the 7205/ 7230 site alone could be transactivated by PAX2. These ®ndings suggest that PAX2 is a tissue-speci®c modulator of WT1 expression, and is involved in cell growth control via WT1.

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Sequence of the WT1 Upstream Region Including the Wit-1 Gene

Cited by 20 publications

References 9 publications

Alternately spliced WT1 antisense transcripts interact with WT1 sense RNA and show epigenetic and splicing defects in cancer

Alternately spliced WT1 antisense transcripts interact with WT1 sense RNA and show epigenetic and splicing defects in cancer

Anti-apoptotic quinolinate phosphoribosyltransferase ( QPRT ) is a target gene of Wilms' tumor gene 1 (WT1) protein in leukemic cells

Differential regulation of the human Wilms tumour suppressor gene (WT1) promoter by two isoforms of PAX2

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