RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/17635184http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17635184http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17635184http://www.w3.org/2000/01/rdf-schema#comment"Drug disposition and response are greatly determined by the activities of drug-metabolizing enzymes and transporters. While the knowledge in terms of CYP enzymes and efflux ABC transporters (such as MDR1, P-glycoprotein) is quite extensive, influx transporters are increasingly being unveiled as key contributors to the process of drug disposition. There is little information on the regulation of these proteins in human cells, especially as regards the effect of endogenous compounds. In this study, we analysed the expression of CYP3A4 and three uptake transporters NTCP (SLC10A1), OATP-A/OATP1A2 (SLCO1A2) and OCT-1 (SLC22A1) in HepG2 cells following treatment with cholesterol. While CYP3A4 and OATP1A2 expression was unaffected, cholesterol treatment led to increased levels of NTCP and OCT-1 mRNAs. Alterations in the functional characteristics and/or expression levels of drug transporters in the liver may conceivably contribute to the variability in drug oral bioavailability often observed in the clinical settings."xsd:string
http://purl.uniprot.org/citations/17635184http://purl.org/dc/terms/identifier"doi:10.1111/j.1472-8206.2007.00517.x"xsd:string
http://purl.uniprot.org/citations/17635184http://purl.org/dc/terms/identifier"doi:10.1111/j.1472-8206.2007.00517.x"xsd:string
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/author"Ribeiro V."xsd:string
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/author"Ribeiro V."xsd:string
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/author"Dias V."xsd:string
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/author"Dias V."xsd:string
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/name"Fundam. Clin. Pharmacol."xsd:string
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/name"Fundam. Clin. Pharmacol."xsd:string
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/pages"445-450"xsd:string
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/pages"445-450"xsd:string
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/title"The expression of the solute carriers NTCP and OCT-1 is regulated by cholesterol in HepG2 cells."xsd:string
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/title"The expression of the solute carriers NTCP and OCT-1 is regulated by cholesterol in HepG2 cells."xsd:string
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/volume"21"xsd:string
http://purl.uniprot.org/citations/17635184http://purl.uniprot.org/core/volume"21"xsd:string
http://purl.uniprot.org/citations/17635184http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17635184
http://purl.uniprot.org/citations/17635184http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17635184
http://purl.uniprot.org/citations/17635184http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17635184
http://purl.uniprot.org/citations/17635184http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17635184
http://purl.uniprot.org/uniprot/O15245http://purl.uniprot.org/core/citationhttp://purl.uniprot.org/citations/17635184
http://purl.uniprot.org/uniprot/O15245#attribution-5C9FC221CD74F5A2085EAF79886E98B5http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/17635184