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000130518 0247_ $$2doi$$a10.1016/j.devcel.2015.12.015
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000130518 1001_ $$0P:(DE-He78)29db88277f131ebd333c5a4e60e824f2$$aScholz, Beate$$b0$$eFirst author
000130518 245__ $$aEndothelial RSPO3 Controls Vascular Stability and Pruning through Non-canonical WNT/Ca(2+)/NFAT Signaling.
000130518 260__ $$aCambridge, Mass.$$bCell Press$$c2016
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000130518 520__ $$aThe WNT signaling enhancer R-spondin3 (RSPO3) is prominently expressed in the vasculature. Correspondingly, embryonic lethality of Rspo3-deficient mice is caused by vessel remodeling defects. Yet the mechanisms underlying vascular RSPO3 function remain elusive. Inducible endothelial Rspo3 deletion (Rspo3-iECKO) resulted in perturbed developmental and tumor vascular remodeling. Endothelial cell apoptosis and vascular pruning led to reduced microvessel density in Rspo3-iECKO mice. Rspo3-iECKO mice strikingly phenocopied the non-canonical WNT signaling-induced vascular defects of mice deleted for the WNT secretion factor Evi/Wls. An endothelial screen for RSPO3 and EVI/WLS co-regulated genes identified Rnf213, Usp18, and Trim30α. RNF213 targets filamin A and NFAT1 for proteasomal degradation attenuating non-canonical WNT/Ca(2+) signaling. Likewise, USP18 and TRIM5α inhibited NFAT1 activation. Consequently, NFAT protein levels were decreased in endothelial cells of Rspo3-iECKO mice and pharmacological NFAT inhibition phenocopied Rspo3-iECKO mice. The data identify endothelial RSPO3-driven non-canonical WNT/Ca(2+)/NFAT signaling as a critical maintenance pathway of the remodeling vasculature.
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000130518 650_7 $$2NLM Chemicals$$aNFATC Transcription Factors
000130518 650_7 $$2NLM Chemicals$$aR-spondin3 protein, mouse
000130518 650_7 $$2NLM Chemicals$$aThrombospondins
000130518 650_7 $$2NLM Chemicals$$aTranscription Factors
000130518 650_7 $$2NLM Chemicals$$aWnt Proteins
000130518 650_7 $$0SY7Q814VUP$$2NLM Chemicals$$aCalcium
000130518 7001_ $$0P:(DE-He78)9f5445b47d46f5f026560c307119a7da$$aKorn, Claudia$$b1
000130518 7001_ $$0P:(DE-He78)adf79fae85fd7368ca32be8adaa63099$$aWojtarowicz, Jessica$$b2
000130518 7001_ $$0P:(DE-He78)18e5b355e4a312d2065b1ae2a9d47654$$aMogler, Carolin$$b3
000130518 7001_ $$0P:(DE-He78)6622aafab3a15676c1ba644a4606decc$$aAugustin, Iris$$b4
000130518 7001_ $$0P:(DE-He78)3c0da8e3caa2aa50cad85152aa0465ad$$aBoutros, Michael$$b5
000130518 7001_ $$0P:(DE-He78)483ad6be7d7fe19e48db9cce86efd70e$$aNiehrs, Christof$$b6
000130518 7001_ $$0P:(DE-He78)2e92d0ae281932fc7347d819fec36b0b$$aAugustin, Hellmut$$b7$$eLast author
000130518 773__ $$0PERI:(DE-600)2053870-4$$a10.1016/j.devcel.2015.12.015$$gVol. 36, no. 1, p. 79 - 93$$n1$$p79 - 93$$tDevelopmental cell$$v36$$x1534-5807$$y2016
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