Ectopic notch activation in developing podocytes causes glomerulosclerosis. - Wikidata - wikimedia - TriplyDB

Ectopic notch activation in developing podocytes causes glomerulosclerosis.

Ectopic notch activation in developing podocytes causes glomerulosclerosis.

http://www.wikidata.org/entity/Q38626505

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The kinetochore protein, CENPF, is mutated in human ciliopathy and microcephaly phenotypes Podocytes Kick it up a notch: Notch signaling and kidney fibrosis Cell biology and pathology of podocytes Key Fibrogenic Signaling Angiotensin II contributes to renal fibrosis independently of Notch pathway activation Genetic Background is a Key Determinant of Glomerular Extracellular Matrix Composition and Organization Slit2 prevents neutrophil recruitment and renal ischemia-reperfusion injury Paraquat poisoning induced pulmonary epithelial mesenchymal transition through Notch1 pathway.ADAM10 is expressed in human podocytes and found in urinary vesicles of patients with glomerular kidney diseases Reduced Notch signaling leads to renal cysts and papillary microadenomas.Autophagy is involved in mouse kidney development and podocyte differentiation regulated by Notch signalling.Proteinuria: an enzymatic disease of the podocyte?Modulation of notch-1 signaling alleviates vascular endothelial growth factor-mediated diabetic nephropathy.Getting a notch closer to understanding diabetic kidney disease.Up-regulation of the homophilic adhesion molecule sidekick-1 in podocytes contributes to glomerulosclerosis Epithelial Notch signaling regulates interstitial fibrosis development in the kidneys of mice and humans Notch activation differentially regulates renal progenitors proliferation and differentiation toward the podocyte lineage in glomerular disorders Activation of Notch signaling pathway in HIV-associated nephropathy.Advances in the biology and genetics of the podocytopathies: implications for diagnosis and therapy The story of Notch and chronic kidney disease.Expression of Notch pathway proteins correlates with albuminuria, glomerulosclerosis, and renal function Notch pathway activation can replace the requirement for Wnt4 and Wnt9b in mesenchymal-to-epithelial transition of nephron stem cells Inhibition of the protein kinase MK-2 protects podocytes from nephrotic syndrome-related injury New insights into epithelial-mesenchymal transition in kidney fibrosis.Effect of Tongxinluo on Nephrin Expression via Inhibition of Notch1/Snail Pathway in Diabetic Rats Epithelial-mesenchymal transition and fibrosis are mutually exclusive reponses in shear-activated proximal tubular epithelial cells.Repair problems in podocytes: Wnt, Notch, and glomerulosclerosis.Notch1 and Notch2 in Podocytes Play Differential Roles During Diabetic Nephropathy Development Inhibition of Notch pathway attenuates the progression of human immunodeficiency virus-associated nephropathy.Notch signaling in diabetic nephropathy Circulating and urinary microRNA profile in focal segmental glomerulosclerosis: a pilot study The fate of Notch-deficient nephrogenic progenitor cells during metanephric kidney development Increased Wnt and Notch signaling: a clue to the renal disease in Schimke immuno-osseous dysplasia?Downregulation of microRNA-30 facilitates podocyte injury and is prevented by glucocorticoids.Childhood nephrotic syndrome--current and future therapies.New insights into the mechanism of notch signalling in fibrosis.Signaling pathways of PAX2 and its role in renal interstitial fibrosis and glomerulosclerosis.Absence of miR-146a in Podocytes Increases Risk of Diabetic Glomerulopathy via Up-regulation of ErbB4 and Notch-1.Understanding podocytopathy and its relevance to clinical nephrology.

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P2860

Ectopic notch activation in developing podocytes causes glomerulosclerosis.

http://www.wikidata.org/entity/Q38626505

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

@zh

2008年论文

@zh-cn

name

Ectopic notch activation in developing podocytes causes glomerulosclerosis.

@en

type

label

Ectopic notch activation in developing podocytes causes glomerulosclerosis.

@en

prefLabel

Ectopic notch activation in developing podocytes causes glomerulosclerosis.

@en

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P1433

Journal of the American Society of Nephrology

P1476

Ectopic notch activation in developing podocytes causes glomerulosclerosis

@en

P2093

Aoife M Waters

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

Corrinne G Lobe

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

Jacob Scutaru

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

Ju Liu

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

Megan Y J Wu

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

Susan E Quaggin

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

Tino D Piscione

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

P2860

MAML1, a human homologue of Drosophila mastermind, is a transcriptional co-activator for NOTCH receptors

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

NOTCH2 mutations cause Alagille syndrome, a heterogeneous disorder of the notch signaling pathway

Segmental expression of Notch and Hairy genes in nephrogenesis

Nck adaptor proteins link nephrin to the actin cytoskeleton of kidney podocytes

Activated notch inhibits myogenic activity of the MADS-Box transcription factor myocyte enhancer factor 2C

Notch signaling controls multiple steps of pancreatic differentiation

Mastermind mediates chromatin-specific transcription and turnover of the Notch enhancer complex

A mouse model of Alagille syndrome: Notch2 as a genetic modifier of Jag1 haploinsufficiency

Notch-1 signalling requires ligand-induced proteolytic release of intracellular domain

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1139-1157

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10.1681/ASN.2007050596

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6

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19

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2396929

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