Source:http://linkedlifedata.com/resource/pubmed/id/11913732
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2002-3-26
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pubmed:abstractText |
Orange et al reported an allelic variant of the human histamine H2 receptor, in which adenine 649 was replaced with guanine, to be more frequent in the schizophrenic population than controls in British Caucasians. The A649 to G change causes an Asn to Asp transition at amino acid position 217 in the third intracellular region, which is postulated to be important for receptor function. Herein, we analyzed the functional significance of this variant using wild-type and variant receptors expressed in Chinese hamster ovary cells. The variant receptor was associated with markedly lower basal cAMP productions than the wild-type receptor. Histamine-dependent cAMP productions via the variant receptor were lower as well. Treatment of cells expressing variant receptors with 10(-5) M ranitidine for 24 h resulted in a reduced degree of receptor upregulation as compared with the wild-type receptor. Thus, this is the first report of an allelic variant of the human H2 receptor which confers altered receptor function. To analyze gastric acid secretion in individuals with this variant, we examined 100 Japanese control subjects. However, neither heterozygotes nor homozygotes were found, suggesting that this variant, if present, is uncommon in the Japanese population.
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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/Cimetidine,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Histamine,
http://linkedlifedata.com/resource/pubmed/chemical/Histamine H2 Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Histamine H2,
http://linkedlifedata.com/resource/pubmed/chemical/tiotidine
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pubmed:status |
MEDLINE
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pubmed:issn |
1470-269X
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pubmed:author |
pubmed-author:AnaiMM,
pubmed-author:AsanoTT,
pubmed-author:FujishiroMM,
pubmed-author:FukushimaYY,
pubmed-author:FunakiMM,
pubmed-author:InukaiKK,
pubmed-author:IshikawaTT,
pubmed-author:NagaiRR,
pubmed-author:OgiharaTT,
pubmed-author:OmataMM,
pubmed-author:OnishiYY,
pubmed-author:OnoHH,
pubmed-author:SaitohTT,
pubmed-author:SakodaHH,
pubmed-author:TsukudaKK
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pubmed:issnType |
Print
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pubmed:volume |
1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
78-83
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pubmed:dateRevised |
2005-11-17
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pubmed:meshHeading |
pubmed-meshheading:11913732-Alleles,
pubmed-meshheading:11913732-Animals,
pubmed-meshheading:11913732-CHO Cells,
pubmed-meshheading:11913732-Cimetidine,
pubmed-meshheading:11913732-Cricetinae,
pubmed-meshheading:11913732-Cyclic AMP,
pubmed-meshheading:11913732-Histamine,
pubmed-meshheading:11913732-Histamine H2 Antagonists,
pubmed-meshheading:11913732-Humans,
pubmed-meshheading:11913732-Mutation,
pubmed-meshheading:11913732-Receptors, Histamine H2,
pubmed-meshheading:11913732-Up-Regulation
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pubmed:year |
2001
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pubmed:articleTitle |
G649, an allelic variant of the human H2 receptor with low basal activity, is resistant to upregulation upon antagonist exposure.
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pubmed:affiliation |
Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan. fksm@tm.kcom.ne.jp
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pubmed:publicationType |
Journal Article
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