The Wt1+/R394W mouse displays glomerulosclerosis and early-onset renal failure characteristic of human Denys-Drash syndrome. - Wikidata - wikimedia - TriplyDB

The Wt1+/R394W mouse displays glomerulosclerosis and early-onset renal failure characteristic of human Denys-Drash syndrome.

The Wt1+/R394W mouse displays glomerulosclerosis and early-onset renal failure characteristic of human Denys-Drash syndrome.

http://www.wikidata.org/entity/Q37598789

about

Deducing the stage of origin of Wilms' tumours from a developmental series of Wt1-mutant mice Hemolytic uremic syndrome as the presenting manifestation of WT1 mutation and Denys-Drash syndrome: a case report.Transcriptomic analysis brings new insight into the biological role of the prion protein during mouse embryogenesis Molecular genetics of Müllerian duct formation, regression and differentiation Disruption of genital ridge development causes aberrant primordial germ cell proliferation but does not affect their directional migration The Wilms tumor gene, Wt1, is critical for mouse spermatogenesis via regulation of sertoli cell polarity and is associated with non-obstructive azoospermia in humans.The Wilms tumor gene, Wt1, is required for Sox9 expression and maintenance of tubular architecture in the developing testis.The yin and yang of kidney development and Wilms' tumors A novel missense mutation of Wilms' Tumor 1 causes autosomal dominant FSGS.New insights into the function of the Wilms tumor suppressor gene WT1 in podocytes.Educational paper: the podocytopathies.Engineering subtle targeted mutations into the mouse genome.Wt1 in the kidney--a tale in mouse models.Ectopic notch activation in developing podocytes causes glomerulosclerosis.Wt1 is involved in leydig cell steroid hormone biosynthesis by regulating paracrine factor expression in mice.Nephrin Tyrosine Phosphorylation Is Required to Stabilize and Restore Podocyte Foot Process Architecture.WT1 Is Necessary for the Proliferation and Migration of Cells of Renin Lineage Following Kidney Podocyte Depletion.Wt1 functions in ovarian follicle development by regulating granulosa cell differentiation.A familial WT1 mutation associated with incomplete Denys-Drash syndrome.Sirolimus interacts with pathways essential for podocyte integrity.Clinical Aspects of WT1 and the Kidney.Knock-in of the R394W mutation causes MDS and cooperates with to drive aggressive myeloid neoplasms in mice

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The Wt1+/R394W mouse displays glomerulosclerosis and early-onset renal failure characteristic of human Denys-Drash syndrome.

http://www.wikidata.org/entity/Q37598789

description

2004 nî lūn-bûn

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2004年の論文

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2004年学术文章

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2004年学术文章

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2004年学术文章

@zh-hans

2004年学术文章

@zh-my

2004年学术文章

@zh-sg

2004年學術文章

@yue

2004年學術文章

@zh

2004年學術文章

@zh-hant

name

The Wt1+/R394W mouse displays ...... of human Denys-Drash syndrome.

@en

The Wt1+/R394W mouse displays ...... of human Denys-Drash syndrome.

@nl

type

label

The Wt1+/R394W mouse displays ...... of human Denys-Drash syndrome.

@en

The Wt1+/R394W mouse displays ...... of human Denys-Drash syndrome.

@nl

prefLabel

The Wt1+/R394W mouse displays ...... of human Denys-Drash syndrome.

@en

The Wt1+/R394W mouse displays ...... of human Denys-Drash syndrome.

@nl

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MCB.24.22.9899-9910.2004

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Molecular and Cellular Biology

P1476

The Wt1+/R394W mouse displays ...... of human Denys-Drash syndrome.

@en

P2093

Fei Gao

http://www.w3.org/2001/XMLSchema#string

Guizhi Sun

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Jian Min Deng

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Malini Udtha

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Nelson G Ordonez

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Richard R Behringer

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Sourindra Maiti

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Vicki Huff

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P2860

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

Upregulation of c-MYC in WT1-mutant tumors: assessment of WT1 putative transcriptional targets using cDNA microarray expression profiling of genetically defined Wilms' tumors

Positionally cloned gene for a novel glomerular protein--nephrin--is mutated in congenital nephrotic syndrome

Wilms' tumor 1 and Dax-1 modulate the orphan nuclear receptor SF-1 in sex-specific gene expression

Loss of glomerular foot processes is associated with uncoupling of podocalyxin from the actin cytoskeleton

Anuria, omphalocele, and perinatal lethality in mice lacking the CD34-related protein podocalyxin

NPHS2, encoding the glomerular protein podocin, is mutated in autosomal recessive steroid-resistant nephrotic syndrome

Mutations in ACTN4, encoding alpha-actinin-4, cause familial focal segmental glomerulosclerosis

CD2-associated protein haploinsufficiency is linked to glomerular disease susceptibility

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

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9899-9910

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scholarly article

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10.1128/MCB.24.22.9899-9910.2004

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22

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525476

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