Source:http://linkedlifedata.com/resource/pubmed/id/20382697
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2010-5-21
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pubmed:abstractText |
Natriuretic peptide receptor-A (NPR-A), also known as guanylyl cyclase-A, is a transmembrane receptor guanylyl cyclase that is activated by the cardiac hormones atrial natriuretic peptide and B-type natriuretic peptide. Although ligand-dependent NPR-A degradation (also known as down-regulation) is widely acknowledged in human and animal models of volume overload, down-regulation in cultured cells is controversial. Here, we examined the effect of ANP exposure on cellular NPR-A levels as a function of time. Relative receptor concentrations were estimated using guanylyl cyclase and immunoblot assays in a wide variety of cell lines that endogenously or exogenously expressed low or high numbers of receptors. ANP exposures of 1 h markedly reduced hormone-dependent but not detergent-dependent guanylyl cyclase activities in membranes from exposed cells. However, 1-h ANP exposures did not significantly reduce NPR-A concentrations in any cell line. In contrast, exposures of greater than 1 h reduced receptor concentrations in a time-dependent manner. The time required for half of the receptors to be degraded (t(1/2)) in primary bovine aortic endothelial and immortalized HeLa cells was approximately 8 h. In contrast, a 24-h exposure of ANP to 293T cells stably overexpressing NPR-A caused less than half of the receptors to be degraded. To our knowledge, this is the first report to directly measure NPR-A down-regulation in endogenously expressing cells. We conclude that down-regulation is a universal property of NPR-A but is relatively slow and varies with receptor expression levels and cell type.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Atrial Natriuretic Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Guanylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Atrial Natriuretic Factor,
http://linkedlifedata.com/resource/pubmed/chemical/atrial natriuretic factor receptor A
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1945-7170
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
151
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2769-76
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pubmed:meshHeading |
pubmed-meshheading:20382697-Animals,
pubmed-meshheading:20382697-Atrial Natriuretic Factor,
pubmed-meshheading:20382697-Cattle,
pubmed-meshheading:20382697-Cell Line,
pubmed-meshheading:20382697-Cell Membrane,
pubmed-meshheading:20382697-Guanylate Cyclase,
pubmed-meshheading:20382697-HeLa Cells,
pubmed-meshheading:20382697-Humans,
pubmed-meshheading:20382697-Immunoblotting,
pubmed-meshheading:20382697-Immunoprecipitation,
pubmed-meshheading:20382697-RNA, Small Interfering,
pubmed-meshheading:20382697-Radioimmunoassay,
pubmed-meshheading:20382697-Rats,
pubmed-meshheading:20382697-Receptors, Atrial Natriuretic Factor
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pubmed:year |
2010
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pubmed:articleTitle |
Prolonged atrial natriuretic peptide exposure stimulates guanylyl cyclase-a degradation.
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pubmed:affiliation |
University of Minnesota Twin Cities, Department of Biochemistry, Molecular Biology, and Biophysics, 6-155 Jackson Hall, 321 Church Street, South East Minneapolis, Minnesota 55455, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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