pubmed-article:17360684 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17360684 | lifeskim:mentions | umls-concept:C0007012 | lld:lifeskim |
pubmed-article:17360684 | lifeskim:mentions | umls-concept:C1853126 | lld:lifeskim |
pubmed-article:17360684 | lifeskim:mentions | umls-concept:C0013138 | lld:lifeskim |
pubmed-article:17360684 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:17360684 | pubmed:dateCreated | 2007-3-15 | lld:pubmed |
pubmed-article:17360684 | pubmed:abstractText | CO(2) elicits a response from many insects, including mosquito vectors of diseases such as malaria and yellow fever, but the molecular basis of CO(2) detection is unknown in insects or other higher eukaryotes. Here we show that Gr21a and Gr63a, members of a large family of Drosophila seven-transmembrane-domain chemoreceptor genes, are coexpressed in chemosensory neurons of both the larva and the adult. The two genes confer CO(2) response when coexpressed in an in vivo expression system, the "empty neuron system." The response is highly specific for CO(2) and dependent on CO(2) concentration. The response shows an equivalent dependence on the dose of Gr21a and Gr63a. None of 39 other chemosensory receptors confers a comparable response to CO(2). The identification of these receptors may now allow the identification of agents that block or activate them. Such agents could affect the responses of insect pests to the humans they seek. | lld:pubmed |
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pubmed-article:17360684 | pubmed:language | eng | lld:pubmed |
pubmed-article:17360684 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17360684 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17360684 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17360684 | pubmed:month | Feb | lld:pubmed |
pubmed-article:17360684 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:17360684 | pubmed:author | pubmed-author:WeissLinnea... | lld:pubmed |
pubmed-article:17360684 | pubmed:author | pubmed-author:CarlsonJohn... | lld:pubmed |
pubmed-article:17360684 | pubmed:author | pubmed-author:KwonJae... | lld:pubmed |
pubmed-article:17360684 | pubmed:author | pubmed-author:DahanukarAnup... | lld:pubmed |
pubmed-article:17360684 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17360684 | pubmed:day | 27 | lld:pubmed |
pubmed-article:17360684 | pubmed:volume | 104 | lld:pubmed |
pubmed-article:17360684 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17360684 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17360684 | pubmed:pagination | 3574-8 | lld:pubmed |
pubmed-article:17360684 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:17360684 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17360684 | pubmed:articleTitle | The molecular basis of CO2 reception in Drosophila. | lld:pubmed |
pubmed-article:17360684 | pubmed:affiliation | Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, CT 06520-8103, USA. | lld:pubmed |
pubmed-article:17360684 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17360684 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:17360684 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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