http://purl.uniprot.org/citations/26766444 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/26766444 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/26766444 | http://www.w3.org/2000/01/rdf-schema#comment | "The WNT signaling enhancer R-spondin3 (RSPO3) is prominently expressed in the vasculature. Correspondingly, embryonic lethality of Rspo3-deficient mice is caused by vessel remodeling defects. Yet the mechanisms underlying vascular RSPO3 function remain elusive. Inducible endothelial Rspo3 deletion (Rspo3-iECKO) resulted in perturbed developmental and tumor vascular remodeling. Endothelial cell apoptosis and vascular pruning led to reduced microvessel density in Rspo3-iECKO mice. Rspo3-iECKO mice strikingly phenocopied the non-canonical WNT signaling-induced vascular defects of mice deleted for the WNT secretion factor Evi/Wls. An endothelial screen for RSPO3 and EVI/WLS co-regulated genes identified Rnf213, Usp18, and Trim30α. RNF213 targets filamin A and NFAT1 for proteasomal degradation attenuating non-canonical WNT/Ca(2+) signaling. Likewise, USP18 and TRIM5α inhibited NFAT1 activation. Consequently, NFAT protein levels were decreased in endothelial cells of Rspo3-iECKO mice and pharmacological NFAT inhibition phenocopied Rspo3-iECKO mice. The data identify endothelial RSPO3-driven non-canonical WNT/Ca(2+)/NFAT signaling as a critical maintenance pathway of the remodeling vasculature."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.devcel.2015.12.015"xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.devcel.2015.12.015"xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Boutros M."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Boutros M."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Augustin H.G."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Augustin H.G."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Augustin I."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Augustin I."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Scholz B."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Scholz B."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Niehrs C."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Niehrs C."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Korn C."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Korn C."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Mogler C."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Mogler C."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Wojtarowicz J."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/author | "Wojtarowicz J."xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/name | "Dev. Cell"xsd:string |
http://purl.uniprot.org/citations/26766444 | http://purl.uniprot.org/core/name | "Dev. Cell"xsd:string |