Proteolytic cleavage of versican during cardiac cushion morphogenesis. - Wikidata - wikimedia - TriplyDB

Proteolytic cleavage of versican during cardiac cushion morphogenesis.

Proteolytic cleavage of versican during cardiac cushion morphogenesis.

http://www.wikidata.org/entity/Q42913840

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A disintegrin-like and metalloprotease (reprolysin-type) with thrombospondin type 1 motif (ADAMTS) superfamily: functions and mechanisms Decellularized matrices for cardiovascular tissue engineering Impact of laminitis on the canonical Wnt signaling pathway in basal epithelial cells of the equine digital laminae Galnt1 is required for normal heart valve development and cardiac function Endothelial deletion of murine Jag1 leads to valve calcification and congenital heart defects associated with Alagille syndrome Transforming growth factor Beta2 is required for valve remodeling during heart development Proteomic-based detection of a protein cluster dysregulated during cardiovascular development identifies biomarkers of congenital heart defects Endocardial Brg1 represses ADAMTS1 to maintain the microenvironment for myocardial morphogenesis ADAMTS5 Is a Critical Regulator of Virus-Specific T Cell Immunity The pattern of congenital heart defects arising from reduced Tbx5 expression is altered in a Down syndrome mouse model Synthesis and organization of hyaluronan and versican by embryonic stem cells undergoing embryoid body differentiation.The multiple, complex roles of versican and its proteolytic turnover by ADAMTS proteases during embryogenesis.Isolation and purification of versican and analysis of versican proteolysis.Determinants of versican-V1 proteoglycan processing by the metalloproteinase ADAMTS5 Chromatin remodeling in cardiovascular development and physiology.BMP-2 induces versican and hyaluronan that contribute to post-EMT AV cushion cell migration.Imbalanced expression of Vcan mRNA splice form proteins alters heart morphology and cellular protein profiles.Extracellular proteases as targets for drug development Altered versican cleavage in ADAMTS5 deficient mice; a novel etiology of myxomatous valve disease.Insufficient versican cleavage and Smad2 phosphorylation results in bicuspid aortic and pulmonary valves Transcriptional Profiling of Cultured, Embryonic Epicardial Cells Identifies Novel Genes and Signaling Pathways Regulated by TGFβR3 In Vitro.Transcriptional Impact of Rare and Private Copy Number Variants in Hypoplastic Left Heart Syndrome Cartilage link protein 1 (Crtl1), an extracellular matrix component playing an important role in heart development.Plasma fibulin-1 is linked to restrictive filling of the left ventricle and to mortality in patients with aortic valve stenosis Endothelial deletion of ADAM17 in mice results in defective remodeling of the semilunar valves and cardiac dysfunction in adults.Correlation of Versican Expression, Accumulation, and Degradation during Embryonic Development by Quantitative Immunohistochemistry What chick and mouse models have taught us about the role of the endocardium in congenital heart disease.Extracellular matrix and heart development.The functional diversity of essential genes required for mammalian cardiac development.How to make a heart valve: from embryonic development to bioengineering of living valve substitutes.Functional analysis of candidate genes in 2q13 deletion syndrome implicates FBLN7 and TMEM87B deficiency in congenital heart defects and FBLN7 in craniofacial malformations.Provisional matrix: A role for versican and hyaluronan.Fibulin-1 Binds to Fibroblast Growth Factor 8 with High Affinity: EFFECTS ON EMBRYO SURVIVAL.Reduced versican cleavage due to Adamts9 haploinsufficiency is associated with cardiac and aortic anomalies.Versican G1 domain and V3 isoform overexpression results in increased chondrogenesis in the developing chick limb in ovo.The role of versican isoforms V0/V1 in glioma migration mediated by transforming growth factor-beta2.Proteolytic cleavage of versican during limb joint development.Cooperation of two ADAMTS metalloproteases in closure of the mouse palate identifies a requirement for versican proteolysis in regulating palatal mesenchyme proliferation.Versican proteolysis mediates myocardial regression during outflow tract development.Tbx20 regulation of endocardial cushion cell proliferation and extracellular matrix gene expression.

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P2860

Proteolytic cleavage of versican during cardiac cushion morphogenesis.

http://www.wikidata.org/entity/Q42913840

description

2006 nî lūn-bûn

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2006年の論文

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年學術文章

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2006年學術文章

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2006年學術文章

@zh-hant

name

Proteolytic cleavage of versican during cardiac cushion morphogenesis.

@en

Proteolytic cleavage of versican during cardiac cushion morphogenesis.

@nl

type

label

Proteolytic cleavage of versican during cardiac cushion morphogenesis.

@en

Proteolytic cleavage of versican during cardiac cushion morphogenesis.

@nl

prefLabel

Proteolytic cleavage of versican during cardiac cushion morphogenesis.

@en

Proteolytic cleavage of versican during cardiac cushion morphogenesis.

@nl

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Developmental Dynamics

P1476

Proteolytic cleavage of versican during cardiac cushion morphogenesis.

@en

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Bryan P Toole

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Christine B Kern

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Corey H Mjaatvedt

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M Luisa Iruela-Arispe

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Sarah E Fairey

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W Scott Argraves

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Waleed O Twal

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P2860

Fibulin is an extracellular matrix and plasma glycoprotein with repeated domain structure

Characterization of ADAMTS-9 and ADAMTS-20 as a distinct ADAMTS subfamily related to Caenorhabditis elegans GON-1

Disruption of hyaluronan synthase-2 abrogates normal cardiac morphogenesis and hyaluronan-mediated transformation of epithelium to mesenchyme

Primer3 on the WWW for general users and for biologist programmers

The proteoglycans aggrecan and Versican form networks with fibulin-2 through their lectin domain binding

Processing and localization of ADAMTS-1 and proteolytic cleavage of versican during cumulus matrix expansion and ovulation

Versican V1 proteolysis in human aorta in vivo occurs at the Glu441-Ala442 bond, a site that is cleaved by recombinant ADAMTS-1 and ADAMTS-4

Heart-valve mesenchyme formation is dependent on hyaluronan-augmented activation of ErbB2-ErbB3 receptors

Expression of PG-M(V3), an alternatively spliced form of PG-M without a chondroitin sulfate attachment in region in mouse and human tissues

The Cspg2 gene, disrupted in the hdf mutant, is required for right cardiac chamber and endocardial cushion formation

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10.1002/DVDY.20838

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8

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235

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16691565

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