http://purl.uniprot.org/citations/16400024 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/16400024 | http://www.w3.org/2000/01/rdf-schema#comment | "Mouse models for autosomal-dominant polycystic kidney disease (ADPKD), derived from homozygous targeted disruption of Pkd1 gene, generally die in utero or perinatally because of systemic defects. We introduced a loxP site and a loxP-flanked mc1-neo cassette into introns 30 and 34, respectively, of the Pkd1 locus to generate a conditional, targeted mutation. Significantly, before excision of the floxed exons and mc1-neo from the targeted locus by Cre recombinase, mice homozygous for the targeted allele appeared normal at birth but developed polycystic kidney disease with a slower progression than that of Pkd-null mice. Further, the homozygotes continued to produce low levels of full-length Pkd1-encoded protein, suggesting that slight Pkd1 expression is sufficient for renal cyst formation in ADPKD. In this viable model, up-regulation of heparin-binding epidermal growth factor-like growth factor accompanied increased epidermal growth factor receptor signaling, which may be involved in abnormal proliferation of the cyst-lining epithelia. Increased apoptosis in cyst epithelia was only observed in the later period that correlated with the cyst regression. Abnormalities in Na(+)/K(+)-ATPase, aquaporin-2, and vasopressin V2 receptor expression were also identified. This mouse model may be suitable for further studies of progression and therapeutic interventions of ADPKD."xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.org/dc/terms/identifier | "doi:10.2353/ajpath.2006.050342"xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/author | "Li H."xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/author | "Lin Y.T."xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/author | "Wang E."xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/author | "Jiang S.T."xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/author | "Lin H.K."xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/author | "Wang C.K."xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/author | "Chiou Y.Y."xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/author | "Tang M.J."xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/author | "Chi Y.C."xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/name | "Am J Pathol"xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/pages | "205-220"xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/title | "Defining a link with autosomal-dominant polycystic kidney disease in mice with congenitally low expression of Pkd1."xsd:string |
http://purl.uniprot.org/citations/16400024 | http://purl.uniprot.org/core/volume | "168"xsd:string |
http://purl.uniprot.org/citations/16400024 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16400024 |
http://purl.uniprot.org/citations/16400024 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16400024 |
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http://purl.uniprot.org/uniprot/#_D3Z5U6-mappedCitation-16400024 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16400024 |
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