| pubmed-article:17960140 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17960140 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:17960140 | lifeskim:mentions | umls-concept:C0022680 | lld:lifeskim |
| pubmed-article:17960140 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
| pubmed-article:17960140 | lifeskim:mentions | umls-concept:C1155265 | lld:lifeskim |
| pubmed-article:17960140 | lifeskim:mentions | umls-concept:C0086344 | lld:lifeskim |
| pubmed-article:17960140 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:17960140 | pubmed:dateCreated | 2007-12-17 | lld:pubmed |
| pubmed-article:17960140 | pubmed:abstractText | Defects in the primary cilium/basal body complex of renal tubular cells cause polycystic kidney disease (PKD). To uncover pathways associated with disease progression, we determined the kidney transcriptome of 10-day-old severely and mildly affected cpk mice, a model of recessive PKD. In the severe phenotype, the most highly expressed genes were those associated with the innate immune response including many macrophage markers, particularly those associated with a profibrotic alternative activation pathway. Additionally, gene expression of macrophage activators was dominated by the complement system factors including the central complement component 3. Additional studies confirmed increased complement component 3 protein levels in both cystic and non-cystic epithelia in the kidneys of cpk compared to wild-type mice. We also found elevated complement component 3 activation in two other mouse-recessive models and human-recessive PKD. Our results suggest that abnormal complement component 3 activation is a key element of progression in PKD. | lld:pubmed |
| pubmed-article:17960140 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17960140 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17960140 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17960140 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17960140 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17960140 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17960140 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17960140 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17960140 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17960140 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:17960140 | pubmed:issn | 0085-2538 | lld:pubmed |
| pubmed-article:17960140 | pubmed:author | pubmed-author:CuqPP | lld:pubmed |
| pubmed-article:17960140 | pubmed:author | pubmed-author:NovakJJ | lld:pubmed |
| pubmed-article:17960140 | pubmed:author | pubmed-author:WooYY | lld:pubmed |
| pubmed-article:17960140 | pubmed:author | pubmed-author:ZhouJJ | lld:pubmed |
| pubmed-article:17960140 | pubmed:author | pubmed-author:ChurchillG... | lld:pubmed |
| pubmed-article:17960140 | pubmed:author | pubmed-author:SzalaiA JAJ | lld:pubmed |
| pubmed-article:17960140 | pubmed:author | pubmed-author:Guay-Woodford... | lld:pubmed |
| pubmed-article:17960140 | pubmed:author | pubmed-author:MrukAA | lld:pubmed |
| pubmed-article:17960140 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17960140 | pubmed:volume | 73 | lld:pubmed |
| pubmed-article:17960140 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17960140 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17960140 | pubmed:pagination | 63-76 | lld:pubmed |
| pubmed-article:17960140 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
| pubmed-article:17960140 | pubmed:meshHeading | pubmed-meshheading:17960140... | lld:pubmed |
| pubmed-article:17960140 | pubmed:meshHeading | pubmed-meshheading:17960140... | lld:pubmed |
| pubmed-article:17960140 | pubmed:meshHeading | pubmed-meshheading:17960140... | lld:pubmed |
| pubmed-article:17960140 | pubmed:meshHeading | pubmed-meshheading:17960140... | lld:pubmed |
| pubmed-article:17960140 | pubmed:meshHeading | pubmed-meshheading:17960140... | lld:pubmed |
| pubmed-article:17960140 | pubmed:meshHeading | pubmed-meshheading:17960140... | lld:pubmed |
| pubmed-article:17960140 | pubmed:meshHeading | pubmed-meshheading:17960140... | lld:pubmed |
| pubmed-article:17960140 | pubmed:meshHeading | pubmed-meshheading:17960140... | lld:pubmed |
| pubmed-article:17960140 | pubmed:meshHeading | pubmed-meshheading:17960140... | lld:pubmed |
| pubmed-article:17960140 | pubmed:meshHeading | pubmed-meshheading:17960140... | lld:pubmed |
| pubmed-article:17960140 | pubmed:meshHeading | pubmed-meshheading:17960140... | lld:pubmed |
| pubmed-article:17960140 | pubmed:meshHeading | pubmed-meshheading:17960140... | lld:pubmed |
| pubmed-article:17960140 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:17960140 | pubmed:articleTitle | Overexpression of innate immune response genes in a model of recessive polycystic kidney disease. | lld:pubmed |
| pubmed-article:17960140 | pubmed:affiliation | Division of Genetic and Translational Medicine, Department of Medicine, The University of Alabama at Birmingham, 720 20th Street South, Birmingham, AL 35294, USA. mmrug@uab.edu.br | lld:pubmed |
| pubmed-article:17960140 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17960140 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17960140 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:12879 | entrezgene:pubmed | pubmed-article:17960140 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17960140 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17960140 | lld:pubmed |
