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http://purl.uniprot.org/citations/17804806http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17804806http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17804806http://www.w3.org/2000/01/rdf-schema#comment"Chemotactic cytokines (chemokines) attract immune cells, although their original evolutionary role may relate more closely with embryonic development. We noted differential expression of the chemokine receptor CXCR7 (RDC-1) on marginal zone B cells, a cell type associated with autoimmune diseases. We generated Cxcr7(-/-) mice but found that CXCR7 deficiency had little effect on B cell composition. However, most Cxcr7(-/-) mice died at birth with ventricular septal defects and semilunar heart valve malformation. Conditional deletion of Cxcr7 in endothelium, using Tie2-Cre transgenic mice, recapitulated this phenotype. Gene profiling of Cxcr7(-/-) heart valve leaflets revealed a defect in the expression of factors essential for valve formation, vessel protection, or endothelial cell growth and survival. We confirmed that the principal chemokine ligand for CXCR7 was CXCL12/SDF-1, which also binds CXCR4. CXCL12 did not induce signaling through CXCR7; however, CXCR7 formed functional heterodimers with CXCR4 and enhanced CXCL12-induced signaling. Our results reveal a specialized role for CXCR7 in endothelial biology and valve development and highlight the distinct developmental role of evolutionary conserved chemokine receptors such as CXCR7 and CXCR4."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0702229104"xsd:string
http://purl.uniprot.org/citations/17804806http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0702229104"xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Li M."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Li M."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Batten M."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Batten M."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Biben C."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Biben C."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Groom J."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Groom J."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Harvey R.P."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Harvey R.P."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Leung H."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Leung H."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Mackay C.R."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Mackay C.R."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Mackay F."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Mackay F."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Martinez-A C."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Martinez-A C."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Martinez-Munoz L."xsd:string
http://purl.uniprot.org/citations/17804806http://purl.uniprot.org/core/author"Martinez-Munoz L."xsd:string