WT1 and glomerular diseases (Q28259503)

https://scigraph.springernature.com/pub.10.1007/s00467-006-0208-1

Europe PubMed Central

title

WT1 and glomerular diseases (English)

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Marie-Claire Gubler

2

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Patrick Niaudet

series ordinal

1

object named as

Patrick Niaudet

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language of work or name

English

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publication date

November 2006

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published in

Pediatric Nephrology

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volume

21

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page(s)

1653-60

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issue

11

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exact match

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cites work

Isolation, characterization, and expression of the murine Wilms' tumor gene (WT1) during kidney development

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DNA recognition by splicing variants of the Wilms' tumor suppressor, WT1

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WT1 and PAX-2 podocyte expression in Denys-Drash syndrome and isolated diffuse mesangial sclerosis

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Diffuse mesangial sclerosis: a congenital glomerulopathy with nephrotic syndrome.

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Human laminin beta2 deficiency causes congenital nephrosis with mesangial sclerosis and distinct eye abnormalities

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Identification of constitutional WT1 mutations, in patients with isolated diffuse mesangial sclerosis, and analysis of genotype/phenotype correlations by use of a computerized mutation database

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Further evidence that imbalance of WT1 isoforms may be involved in Denys – Drash syndrome

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A clinical overview of WT1 gene mutations

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Del 11p/aniridia complex. Report of three patients and review of 37 observations from the literature

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Subnuclear localization of WT1 in splicing or transcription factor domains is regulated by alternative splicing

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Clinicopathologic review of twelve children with nephropathy, Wilms tumor, and genital abnormalities (Drash syndrome).

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Mother-to-child transmitted WT1 splice-site mutation is responsible for distinct glomerular diseases

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Spectrum of early onset nephrotic syndrome associated with WT1 missense mutations.

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Isolated diffuse mesangial sclerosis and Wilms tumor suppressor gene

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Familial Wilms' tumor associated with a WT1 zinc finger mutation

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A girl with bilateral ovarian tumours: Frasier syndrome.

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WT1 splice site mutation in a 46,XX female with minimal-change nephrotic syndrome and Wilms' tumour

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Evidence for the genetic heterogeneity of nephropathic phenotypes associated with Denys-Drash and Frasier syndromes

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Do intronic mutations affecting splicing of WT1 exon 9 cause Frasier syndrome?

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Bilateral Wilms tumor in a boy with severe hypospadias and cryptochidism due to a heterozygous mutation in the WT1 gene

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46,XY phenotypic male with focal segmental glomerulosclerosis caused by the WT1 splice site mutation

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Frasier syndrome, part of the Denys Drash continuum or simply a WT1 gene associated disorder of intersex and nephropathy?

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Renal failure in the Denys-Drash and Wilms' tumor-aniridia syndromes

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WT1 splice-site mutations are rarely associated with primary steroid-resistant focal and segmental glomerulosclerosis.

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A syndrome of pseudohermaphroditism, Wilms' tumor, hypertension, and degenerative renal disease

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A non-AUG translational initiation event generates novel WT1 isoforms

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The same mutation affecting the splicing ofWT1 gene is present on Frasier syndrome patients with or without Wilms' tumor

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Frasier syndrome: a cause of focal segmental glomerulosclerosis in a 46,XX female.

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WT1 mutations associated with incomplete Denys-Drash syndrome define a domain predicted to behave in a dominant-negative fashion

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The Wilms' tumor gene product WT1 activates or suppresses transcription through separate functional domains

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

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Antagonism of WT1 activity by protein self-association.

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A WT1 exon 1 mutation in a child diagnosed with Denys-Drash syndrome

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Nephropathy-gonadal dysgenesis, type 2: renal failure in three siblings with XY dysgenesis in one

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A zinc finger truncation of murine WT1 results in the characteristic urogenital abnormalities of Denys-Drash syndrome

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Deregulation of Pax-2 expression in transgenic mice generates severe kidney abnormalities.

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Inherited WT1 mutation in Denys-Drash syndrome

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Constitutional WT1 mutations in Wilms' tumor patients

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Prophylactic bilateral nephrectomies in two paediatric patients with missense mutations in the WT1 gene

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Germline mutations in the Wilms' tumor suppressor gene are associated with abnormal urogenital development in Denys-Drash syndrome

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Absent pubertal development in a child with chronic renal failure: the case of Frasier syndrome

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The genomic organization and expression of the WT1 gene

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Frasier syndrome is caused by defective alternative splicing of WT1 leading to an altered ratio of WT1 +/-KTS splice isoforms.

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Donor splice-site mutations in WT1 are responsible for Frasier syndrome

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Diaphragmatic hernia in Denys-Drash syndrome

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Frasier syndrome comes full circle: genetic studies performed in an original patient.

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A Japanese case with Frasier syndrome caused by the splice junction mutation of WT1 gene

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A novel missense mutation of the Wt1 gene causing Denys-Drash syndrome with exceptionally mild renal manifestations

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Homozygous deletion in Wilms tumours of a zinc-finger gene identified by chromosome jumping

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Two cases of isolated diffuse mesangial sclerosis with WT1 mutations

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Gonadal mosaicism of Frasier syndrome in 3 Chinese siblings with donor splice site mutation of Wilms' tumour gene

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WT1 is a key regulator of podocyte function: reduced expression levels cause crescentic glomerulonephritis and mesangial sclerosis

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GONADOBLASTOMA ASSOCIATED WITH PURE GONADAL DYSGENESIS IN MONOZYGOUS TWINS.

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12 December 2020

Exon 9 mutations in the WT1 gene, without influencing KTS splice isoforms, are also responsible for Frasier syndrome

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12 December 2020

Frasier syndrome with childhood-onset renal failure

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12 December 2020

WT1, renal development, and glomerulopathies

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RNA editing in the Wilms' tumor susceptibility gene, WT1

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Germline intronic and exonic mutations in the Wilms' tumour gene (WT1) affecting urogenital development

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Novel familial WT1 read-through mutation associated with Wilms tumor and slow progressive nephropathy.

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Alternative splicing and genomic structure of the Wilms tumor gene WT1

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Mutations in the Wilms' tumor 1 gene cause isolated steroid resistant nephrotic syndrome and occur in exons 8 and 9.

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12 December 2020

10.1007/S00467-006-0208-1

Identifiers

DOI

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Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

3685240

Dimensions Publication ID

1022484112

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OpenCitations bibliographic resource ID

3685240

1 reference