Source:http://linkedlifedata.com/resource/pubmed/id/11841625
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1 Suppl
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pubmed:dateCreated |
2002-2-13
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pubmed:abstractText |
Several aquaporin- (AQP) type water channels are expressed in kidney tubules and microvessels, including AQP1 in proximal tubule, thin descending limb of Henle and vasa recta, AQP2 in collecting duct apical membrane, and AQP3 and AQP4 in collecting duct basolateral membrane. Mice deficient in these aquaporins have distinct phenotypic abnormalities. AQP1 null mice are polyuria and unable to generate a concentrated urine after water deprivation. AQP2-T126M mutant mice and AQP3 null mice manifest nephrogenic diabetes insipidus (NDI) with severe polyuria, whereas AQP4 null mice have only a mild defect in maximal urinary concentrating ability. We reasoned that these mice could serve as useful models for gene replacement because of their predictable and unambiguous phenotypes.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1523-1755
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
61
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
S120-4
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pubmed:meshHeading | |
pubmed:year |
2002
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pubmed:articleTitle |
Aquaporin gene delivery to kidney.
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pubmed:affiliation |
Department of Medicine, Cardiovascular Research Institute, University of California, San Francisco, CA 94143-0521, USA. verkman@itsa.ucsf.edu
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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