Source:http://linkedlifedata.com/resource/pubmed/id/18358473
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
2008-3-31
|
| pubmed:abstractText |
Caveolin-1 (cav-1) is a major structural protein of caveolae, small invaginations of the plasma membrane that integrate and regulate signaling pathways involved in cell growth and differentiation. We previously generated a genetically engineered mice that are homozygous for a null mutation in exon 2 of cav-1 and documented increased incidence of urolithiasis in young male cav-1(-/-) mice. We attributed this, in part, to improper localization of plasma membrane calcium/calmodulin-dependent calcium ATPase in the distal convoluted tubules of the kidney. To document pathologies related to cav-1 function, we maintained cav-1(-/-) and control cav-1(+/+) mice for an extended time period. We report here that cav-1(-/-) mice demonstrate organ-specific growth-related disorders in stromal cells that normally have high levels of cav-1 expression. In many of these organs, epithelial cell growth/differentiation abnormalities were also observed, yet in most of these sites the epithelial cells normally express low to non-detectable levels of cav-1. We propose that loss of cav-1 function in stromal cells of various organs directly leads to a disorganized stromal compartment that, in turn, indirectly promotes abnormal growth and differentiation of adjacent epithelium.
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| pubmed:grant | |
| pubmed:commentsCorrections | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Apr
|
| pubmed:issn |
0014-4800
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| pubmed:author |
pubmed-author:CaoGuangwenG,
pubmed-author:FattahEl Moataz Abdelel MA,
pubmed-author:FujitaTetsuoT,
pubmed-author:GuangYangY,
pubmed-author:NaruishiKojiK,
pubmed-author:RajagopalanKartikK,
pubmed-author:RajocopolanKartikK,
pubmed-author:ThompsonTimothy CTC,
pubmed-author:TimmeTerry LTL,
pubmed-author:TroungLuan DLD
|
| pubmed:issnType |
Print
|
| pubmed:volume |
84
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
131-40
|
| pubmed:dateRevised |
2010-7-14
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| pubmed:meshHeading |
pubmed-meshheading:18358473-Animals,
pubmed-meshheading:18358473-Biological Markers,
pubmed-meshheading:18358473-Caveolin 1,
pubmed-meshheading:18358473-Cell Differentiation,
pubmed-meshheading:18358473-Epithelial Cells,
pubmed-meshheading:18358473-Female,
pubmed-meshheading:18358473-Gene Expression Regulation,
pubmed-meshheading:18358473-Gene Silencing,
pubmed-meshheading:18358473-Genitalia,
pubmed-meshheading:18358473-Keratins,
pubmed-meshheading:18358473-Longevity,
pubmed-meshheading:18358473-Lung,
pubmed-meshheading:18358473-Male,
pubmed-meshheading:18358473-Mammary Glands, Animal,
pubmed-meshheading:18358473-Mice,
pubmed-meshheading:18358473-Mice, Inbred C57BL,
pubmed-meshheading:18358473-Mice, Knockout,
pubmed-meshheading:18358473-Pancreas,
pubmed-meshheading:18358473-Spleen,
pubmed-meshheading:18358473-Stromal Cells,
pubmed-meshheading:18358473-Urinary Bladder
|
| pubmed:year |
2008
|
| pubmed:articleTitle |
Mice with cav-1 gene disruption have benign stromal lesions and compromised epithelial differentiation.
|
| pubmed:affiliation |
Scott Department of Urology, Baylor College of Medicine, Houston, TX, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, N.I.H., Extramural
|