pubmed-article:16400024 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16400024 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:16400024 | lifeskim:mentions | umls-concept:C0022680 | lld:lifeskim |
pubmed-article:16400024 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:16400024 | lifeskim:mentions | umls-concept:C1418599 | lld:lifeskim |
pubmed-article:16400024 | lifeskim:mentions | umls-concept:C0205251 | lld:lifeskim |
pubmed-article:16400024 | lifeskim:mentions | umls-concept:C1704666 | lld:lifeskim |
pubmed-article:16400024 | lifeskim:mentions | umls-concept:C1517892 | lld:lifeskim |
pubmed-article:16400024 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:16400024 | lifeskim:mentions | umls-concept:C0208973 | lld:lifeskim |
pubmed-article:16400024 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:16400024 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:16400024 | pubmed:dateCreated | 2006-1-9 | lld:pubmed |
pubmed-article:16400024 | pubmed:abstractText | 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. | lld:pubmed |
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pubmed-article:16400024 | pubmed:language | eng | lld:pubmed |
pubmed-article:16400024 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16400024 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:16400024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16400024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:16400024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16400024 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:16400024 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16400024 | pubmed:month | Jan | lld:pubmed |
pubmed-article:16400024 | pubmed:issn | 0002-9440 | lld:pubmed |
pubmed-article:16400024 | pubmed:author | pubmed-author:LiHungH | lld:pubmed |
pubmed-article:16400024 | pubmed:author | pubmed-author:TangMing-JerM... | lld:pubmed |
pubmed-article:16400024 | pubmed:author | pubmed-author:JiangSi-TseST | lld:pubmed |
pubmed-article:16400024 | pubmed:author | pubmed-author:WangChi-Kuang... | lld:pubmed |
pubmed-article:16400024 | pubmed:author | pubmed-author:ChiouYuan-Yow... | lld:pubmed |
pubmed-article:16400024 | pubmed:author | pubmed-author:ChiYing-ChihY... | lld:pubmed |
pubmed-article:16400024 | pubmed:author | pubmed-author:WangEllianE | lld:pubmed |
pubmed-article:16400024 | pubmed:author | pubmed-author:LinHsiu-KuanH... | lld:pubmed |
pubmed-article:16400024 | pubmed:author | pubmed-author:LinYuan-TaYT | lld:pubmed |
pubmed-article:16400024 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16400024 | pubmed:volume | 168 | lld:pubmed |
pubmed-article:16400024 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16400024 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16400024 | pubmed:pagination | 205-20 | lld:pubmed |
pubmed-article:16400024 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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