Source:http://linkedlifedata.com/resource/pubmed/id/16474191
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2006-2-13
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pubmed:abstractText |
Primary cilia are hypothesized to act as a mechanical sensor to detect renal tubular fluid flow. Anomalous structure of primary cilia and/or impairment of increases in intracellular Ca2+ concentration in response to fluid flow are thought to result in renal cyst formation in conditional kif3a knockout, Tg737 and pkd1/pkd2 mutant mice. The mutant inv/inv mouse develops multiple renal cysts like kif3a, Tg737 and pkd1/pkd2 mutants. Inv proteins have been shown to be localized in the renal primary cilia, but response of inv/inv cilia to fluid stress has not been examined. In the present study, we examined the mechanical response of primary cilia to physiological fluid flow using a video microscope, as well as intracellular Ca2+ increases in renal epithelial cells from normal and inv/inv mice in response to flow stress. Percentages of ciliated cells and the length of primary cilia were not significantly different between primary renal cell cultures from normal and inv/inv mutant mice. Localization of inv protein was restricted to the base of primary cilia even under flow stress. Inv/inv mutant cells had similar bending mechanics of primary cilia in response to physiological fluid flow compared to normal cells. Furthermore, no difference was found in intracellular Ca2+ increases in response to physiological fluid flow between normal and inv/inv mutant cells. Our present study suggests that the function of the inv protein is distinct from polaris (the Tg737 gene product), polycystins (pkd1 and pkd2 gene products).
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Invs protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/TRPP Cation Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Tg737Rpw protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/polycystic kidney disease 1 protein,
http://linkedlifedata.com/resource/pubmed/chemical/polycystic kidney disease 2 protein
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pubmed:status |
MEDLINE
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pubmed:issn |
1347-3700
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
30
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
93-100
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pubmed:dateRevised |
2007-10-18
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pubmed:meshHeading |
pubmed-meshheading:16474191-Animals,
pubmed-meshheading:16474191-Calcium,
pubmed-meshheading:16474191-Cells, Cultured,
pubmed-meshheading:16474191-Cilia,
pubmed-meshheading:16474191-Epithelial Cells,
pubmed-meshheading:16474191-Extracellular Fluid,
pubmed-meshheading:16474191-Kidney,
pubmed-meshheading:16474191-Kidney Diseases, Cystic,
pubmed-meshheading:16474191-Membrane Proteins,
pubmed-meshheading:16474191-Mice,
pubmed-meshheading:16474191-Mice, Mutant Strains,
pubmed-meshheading:16474191-Mice, Transgenic,
pubmed-meshheading:16474191-Microscopy, Video,
pubmed-meshheading:16474191-Proteins,
pubmed-meshheading:16474191-TRPP Cation Channels,
pubmed-meshheading:16474191-Transcription Factors,
pubmed-meshheading:16474191-Tumor Suppressor Proteins
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pubmed:year |
2005
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pubmed:articleTitle |
Primary cilia of inv/inv mouse renal epithelial cells sense physiological fluid flow: bending of primary cilia and Ca2+ influx.
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pubmed:affiliation |
Department of Anatomy and Developmental Biology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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