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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2000-1-24
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pubmed:abstractText |
When the wild type beta1-adrenergic receptor (WT-beta1AR) was expressed in Sf9 cells, the beta1AR-stimulated adenylyl cyclase activities were desensitized by prior treatment with isoproterenol. The extent of beta1AR desensitization was not modified, and the onset was not promoted by the overexpression of G protein-coupled receptor kinase 2 (GRK2), GRK5 or GRK6. However, overexpression of the dominant negative mutant of GRK2 appeared to inhibit desensitization of the beta1AR. The change of the potential protein kinase A phosphorylation site located at the intracellular third loop did not affect beta1AR desensitization. Desensitization of the truncated mutant, in which nearly all of the serine and threonine residues from the carboxyl terminus were eliminated, was the same as that of the WT-beta1AR. A deletion mutant that lacked serine and threonine residues of the intracellular third loop was also desensitized by isoproterenol stimulation. Furthermore, the deletion of serine and threonine residues from both the intracellular third loop and carboxyl terminus did not affect desensitization of the beta1AR. These results suggested that phosphorylation by endogenous GRKs in Sf9 cells contributed to desensitization of the beta1AR and that the regions other than third intracellular loop and carboxyl terminus may be responsible for beta1AR desensitization.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrbk1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-1 Receptor Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP-Dependent Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/G-Protein-Coupled Receptor Kinase 2,
http://linkedlifedata.com/resource/pubmed/chemical/G-Protein-Coupled Receptor Kinase 5,
http://linkedlifedata.com/resource/pubmed/chemical/G-Protein-Coupled Receptor Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/G-protein-coupled receptor kinase 6,
http://linkedlifedata.com/resource/pubmed/chemical/GRK5 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Gprk5 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta-1,
http://linkedlifedata.com/resource/pubmed/chemical/beta-Adrenergic Receptor Kinases
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0021-5198
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
81
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
12-20
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:10580365-Adrenergic beta-1 Receptor Agonists,
pubmed-meshheading:10580365-Amino Acid Sequence,
pubmed-meshheading:10580365-Animals,
pubmed-meshheading:10580365-Baculoviridae,
pubmed-meshheading:10580365-Binding Sites,
pubmed-meshheading:10580365-Cyclic AMP-Dependent Protein Kinases,
pubmed-meshheading:10580365-G-Protein-Coupled Receptor Kinase 2,
pubmed-meshheading:10580365-G-Protein-Coupled Receptor Kinase 5,
pubmed-meshheading:10580365-G-Protein-Coupled Receptor Kinases,
pubmed-meshheading:10580365-Humans,
pubmed-meshheading:10580365-Molecular Sequence Data,
pubmed-meshheading:10580365-Mutagenesis, Site-Directed,
pubmed-meshheading:10580365-Phosphorylation,
pubmed-meshheading:10580365-Protein Structure, Tertiary,
pubmed-meshheading:10580365-Protein-Serine-Threonine Kinases,
pubmed-meshheading:10580365-Rats,
pubmed-meshheading:10580365-Receptors, Adrenergic, beta-1,
pubmed-meshheading:10580365-Spodoptera,
pubmed-meshheading:10580365-beta-Adrenergic Receptor Kinases
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pubmed:year |
1999
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pubmed:articleTitle |
Analysis of domain responsible for desensitization of beta1-adrenergic receptor.
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pubmed:affiliation |
Laboratory of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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