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http://purl.uniprot.org/citations/32141129http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32141129http://www.w3.org/2000/01/rdf-schema#comment"Low nephron number results in an increased risk of developing hypertension and chronic kidney disease. Intrauterine growth restriction is associated with a nephron deficit in humans, and is commonly caused by placental insufficiency, which results in fetal hypoxia. The underlying mechanisms by which hypoxia impacts kidney development are poorly understood. microRNA-210 is the most consistently induced microRNA in hypoxia and is known to promote cell survival in a hypoxic environment. In this study, the role of microRNA-210 in kidney development was evaluated using a global microRNA-210 knockout mouse. A male-specific 35% nephron deficit in microRNA-210 knockout mice was observed. Wnt/β-catenin signaling, a pathway crucial for nephron differentiation, was misregulated in male kidneys with increased expression of the canonical Wnt target lymphoid enhancer binding factor 1. This coincided with increased expression of caspase-8-associated protein 2, a known microRNA-210 target and apoptosis signal transducer. Together, these data are consistent with a sex-specific requirement for microRNA-210 in kidney development."xsd:string
http://purl.uniprot.org/citations/32141129http://purl.org/dc/terms/identifier"doi:10.1096/fj.201902767r"xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/author"Ho J."xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/author"Kostka D."xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/author"Cerqueira D.M."xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/author"Hemker S.L."xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/author"Sims-Lucas S."xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/author"Bodnar A.J."xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/author"Clugston A."xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/author"Cargill K.R."xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/author"Anslow M.J."xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/name"FASEB J"xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/pages"5782-5799"xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/title"Deletion of hypoxia-responsive microRNA-210 results in a sex-specific decrease in nephron number."xsd:string
http://purl.uniprot.org/citations/32141129http://purl.uniprot.org/core/volume"34"xsd:string
http://purl.uniprot.org/citations/32141129http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/32141129
http://purl.uniprot.org/citations/32141129http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/32141129
http://purl.uniprot.org/uniprot/#_A0A0G2JDR2-mappedCitation-32141129http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32141129
http://purl.uniprot.org/uniprot/#_A0A0G2JGE9-mappedCitation-32141129http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32141129
http://purl.uniprot.org/uniprot/#_A0A0A6YWU2-mappedCitation-32141129http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32141129
http://purl.uniprot.org/uniprot/#_A0A0A6YWW5-mappedCitation-32141129http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32141129
http://purl.uniprot.org/uniprot/#_A0A0A6YY47-mappedCitation-32141129http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32141129
http://purl.uniprot.org/uniprot/#_A0A0A6YY91-mappedCitation-32141129http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32141129