RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/24904090http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24904090http://www.w3.org/2000/01/rdf-schema#comment"Recombination signal binding protein for Ig-κJ region (RBP-J), the major downstream effector of Notch signaling, is necessary to maintain the number of renin-positive juxtaglomerular cells and the plasticity of arteriolar smooth muscle cells to re-express renin when homeostasis is threatened. We hypothesized that RBP-J controls a repertoire of genes that defines the phenotype of the renin cell. Mice bearing a bacterial artificial chromosome reporter with a mutated RBP-J binding site in the renin promoter had markedly reduced reporter expression at the basal state and in response to a homeostatic challenge. Mice with conditional deletion of RBP-J in renin cells had decreased expression of endocrine (renin and Akr1b7) and smooth muscle (Acta2, Myh11, Cnn1, and Smtn) genes and regulators of smooth muscle expression (miR-145, SRF, Nfatc4, and Crip1). To determine whether RBP-J deletion decreased the endowment of renin cells, we traced the fate of these cells in RBP-J conditional deletion mice. Notably, the lineage staining patterns in mutant and control kidneys were identical, although mutant kidneys had fewer or no renin-expressing cells in the juxtaglomerular apparatus. Microarray analysis of mutant arterioles revealed upregulation of genes usually expressed in hematopoietic cells. Thus, these results suggest that RBP-J maintains the identity of the renin cell by not only activating genes characteristic of the myo-endocrine phenotype but also, preventing ectopic gene expression and adoption of an aberrant phenotype, which could have severe consequences for the control of homeostasis."xsd:string
http://purl.uniprot.org/citations/24904090http://purl.org/dc/terms/identifier"doi:10.1681/asn.2013101045"xsd:string
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/author"Yu J."xsd:string
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/author"Gomez R.A."xsd:string
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/author"Pentz E.S."xsd:string
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/author"Lin E."xsd:string
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/author"Medrano S."xsd:string
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/author"Gross K.W."xsd:string
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/author"Sequeira-Lopez M.L."xsd:string
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/author"Castellanos-Rivera R.M."xsd:string
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/name"J Am Soc Nephrol"xsd:string
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/pages"67-80"xsd:string
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/title"Recombination signal binding protein for Ig-kappaJ region regulates juxtaglomerular cell phenotype by activating the myo-endocrine program and suppressing ectopic gene expression."xsd:string
http://purl.uniprot.org/citations/24904090http://purl.uniprot.org/core/volume"26"xsd:string
http://purl.uniprot.org/citations/24904090http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24904090
http://purl.uniprot.org/citations/24904090http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24904090
http://purl.uniprot.org/uniprot/#_A0A0J9YTV5-mappedCitation-24904090http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24904090
http://purl.uniprot.org/uniprot/#_A0A0J9YVE0-mappedCitation-24904090http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24904090
http://purl.uniprot.org/uniprot/#_A0N920-mappedCitation-24904090http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24904090
http://purl.uniprot.org/uniprot/#_E9Q7W0-mappedCitation-24904090http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24904090
http://purl.uniprot.org/uniprot/#_Q6R5E9-mappedCitation-24904090http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24904090
http://purl.uniprot.org/uniprot/#_P31266-mappedCitation-24904090http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24904090
http://purl.uniprot.org/uniprot/#_Q3U6F1-mappedCitation-24904090http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24904090