| pubmed-article:10571227 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10571227 | lifeskim:mentions | umls-concept:C0113519 | lld:lifeskim |
| pubmed-article:10571227 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:10571227 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:10571227 | lifeskim:mentions | umls-concept:C0162610 | lld:lifeskim |
| pubmed-article:10571227 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:10571227 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:10571227 | pubmed:dateCreated | 1999-12-6 | lld:pubmed |
| pubmed-article:10571227 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10571227 | pubmed:abstractText | We investigated the EGL-30 (Gqalpha) pathway in C. elegans by using genetic screens to identify genes that confer phenotypes similar to egl-30 mutants. One such gene, egl-8, encodes a phospholipase Cbeta that is present throughout the nervous system and near intestinal cell junctions. EGL-30 and EGL-8 appear to positively regulate synaptic transmission because reducing their function results in strong aldicarb resistance and slow locomotion rates. In contrast, GOA-1 (Goalpha) and DGK-1 (diacylglycerol kinase) appear to negatively regulate synaptic transmission, because reducing their function results in strong aldicarb hypersensitivity and hyperactive locomotion. A genetic analysis suggests that GOA-1 negatively regulates the EGL-30 pathway and that DGK-1 antagonizes the EGL-30 pathway. | lld:pubmed |
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| pubmed-article:10571227 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10571227 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10571227 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10571227 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10571227 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:10571227 | pubmed:issn | 0896-6273 | lld:pubmed |
| pubmed-article:10571227 | pubmed:author | pubmed-author:MillerK GKG | lld:pubmed |
| pubmed-article:10571227 | pubmed:author | pubmed-author:RandJ BJB | lld:pubmed |
| pubmed-article:10571227 | pubmed:author | pubmed-author:EmersonM DMD | lld:pubmed |
| pubmed-article:10571227 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10571227 | pubmed:volume | 24 | lld:pubmed |
| pubmed-article:10571227 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10571227 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10571227 | pubmed:pagination | 323-33 | lld:pubmed |
| pubmed-article:10571227 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:10571227 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10571227 | pubmed:articleTitle | Goalpha and diacylglycerol kinase negatively regulate the Gqalpha pathway in C. elegans. | lld:pubmed |
| pubmed-article:10571227 | pubmed:affiliation | Program in Molecular and Cell Biology, Oklahoma Medical Research Foundation, Oklahoma City 73104, USA. | lld:pubmed |
| pubmed-article:10571227 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10571227 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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