The ectodomain of the Notch3 receptor accumulates within the cerebrovasculature of CADASIL patients - Wikidata - wikimedia - TriplyDB

The ectodomain of the Notch3 receptor accumulates within the cerebrovasculature of CADASIL patients

The ectodomain of the Notch3 receptor accumulates within the cerebrovasculature of CADASIL patients

http://www.wikidata.org/entity/Q24629786

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Members of the Jagged/Notch gene families are expressed in injured arteries and regulate cell phenotype via alterations in cell matrix and cell-cell interaction Conserved signal peptide of Notch3 inhibits interaction with proteasome Notch3 signaling promotes the development of pulmonary arterial hypertension A CADASIL-mutated Notch 3 receptor exhibits impaired intracellular trafficking and maturation but normal ligand-induced signaling.CADASIL: Notch signaling defect or protein accumulation problem?Thrombospondin 2 potentiates notch3/jagged1 signaling Cerebral small vessel disease: Capillary pathways to stroke and cognitive decline Impact of notch signaling on inflammatory responses in cardiovascular disorders Exome sequencing reveals an unexpected genetic cause of disease: NOTCH3 mutation in a Turkish family with Alzheimer's disease Endothelial expression of the Notch ligand Jagged1 is required for vascular smooth muscle development Biochemical characterization and cellular effects of CADASIL mutants of NOTCH3 Coordinate Notch3-hairy-related transcription factor pathway regulation in response to arterial injury. Mediator role of platelet-derived growth factor and ERK Stroke Risk Factors, Genetics, and Prevention.Von Willebrand Factor permeates small vessels in CADASIL and inhibits smooth muscle gene expression.Targeting notch pathway enhances rapamycin antitumor activity in pancreas cancers through PTEN phosphorylation Notch3 is a major regulator of vascular tone in cerebral and tail resistance arteries Distinct phenotypic and functional features of CADASIL mutations in the Notch3 ligand binding domain Cerebrovascular dysfunction and microcirculation rarefaction precede white matter lesions in a mouse genetic model of cerebral ischemic small vessel disease Notch signaling respecifies the hemangioblast to a cardiac fate CADASIL and CARASIL.Notch2 and Notch3 function together to regulate vascular smooth muscle development.Role of electron microscopy in the diagnosis of cadasil syndrome: a study of 32 patients Is the oxidant/antioxidant status altered in CADASIL patients?Neuropsychiatric manifestations in CADASIL.Integration of expression profiles and genetic mapping data to identify candidate genes in intracranial aneurysm.Characteristic features of in vivo skin microvascular reactivity in CADASIL.Antibodies that detect O-linked β-D-N-acetylglucosamine on the extracellular domain of cell surface glycoproteins.A switch in Notch gene expression parallels stem cell to endothelial transition in infantile hemangioma.Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: a genetic cause of cerebral small vessel disease.Pathogenic mutations associated with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy differently affect Jagged1 binding and Notch3 activity via the RBP/JK signaling Pathway.A novel cysteine-sparing NOTCH3 mutation in a Chinese family with CADASIL Vascular accumulation of the small leucine-rich proteoglycan decorin in CADASIL.Notch signaling functions in retinal pericyte survival Jagged1 mutations in alagille syndrome.Notch3 is critical for proper angiogenesis and mural cell investment.Identification of a known mutation in Notch 3 in familiar CADASIL in China.Glial vascular degeneration in CADASIL.The pathobiology of vascular malformations: insights from human and model organism genetics.Sequestration of latent TGF-β binding protein 1 into CADASIL-related Notch3-ECD deposits Von Willebrand factor inhibits mature smooth muscle gene expression through impairment of Notch signaling.

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The ectodomain of the Notch3 receptor accumulates within the cerebrovasculature of CADASIL patients

http://www.wikidata.org/entity/Q24629786

description

2000 nî lūn-bûn

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2000 թուականի Մարտին հրատարակուած գիտական յօդուած

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2000 թվականի մարտին հրատարակված գիտական հոդված

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2000年の論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年论文

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The ectodomain of the Notch3 r ...... asculature of CADASIL patients

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The ectodomain of the Notch3 r ...... asculature of CADASIL patients

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The ectodomain of the Notch3 r ...... asculature of CADASIL patients

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The ectodomain of the Notch3 r ...... asculature of CADASIL patients

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The ectodomain of the Notch3 r ...... asculature of CADASIL patients

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P2860

Intracellular cleavage of Notch leads to a heterodimeric receptor on the plasma membrane

Expression patterns of Jagged, Delta1, Notch1, Notch2, and Notch3 genes identify ligand-receptor pairs that may function in neural development

The Notch1 receptor is cleaved constitutively by a furin-like convertase

Notch signaling: cell fate control and signal integration in development

A presenilin-1-dependent gamma-secretase-like protease mediates release of Notch intracellular domain

Strong clustering and stereotyped nature of Notch3 mutations in CADASIL patients

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy maps to chromosome 19q12

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

Notch3 mutations in CADASIL, a hereditary adult-onset condition causing stroke and dementia

The novel Notch homologue mouse Notch 3 lacks specific epidermal growth factor-repeats and is expressed in proliferating neuroepithelium

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597-605

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4208851

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10.1172/JCI8047

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5

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105

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Elisabeth Tournier-Lasserve

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2000-03-01T00:00:00Z

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10712431

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289174

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