| pubmed-article:17404221 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17404221 | lifeskim:mentions | umls-concept:C0020792 | lld:lifeskim |
| pubmed-article:17404221 | lifeskim:mentions | umls-concept:C1513112 | lld:lifeskim |
| pubmed-article:17404221 | lifeskim:mentions | umls-concept:C0205199 | lld:lifeskim |
| pubmed-article:17404221 | lifeskim:mentions | umls-concept:C1883254 | lld:lifeskim |
| pubmed-article:17404221 | lifeskim:mentions | umls-concept:C0243077 | lld:lifeskim |
| pubmed-article:17404221 | pubmed:issue | 15 | lld:pubmed |
| pubmed-article:17404221 | pubmed:dateCreated | 2007-4-11 | lld:pubmed |
| pubmed-article:17404221 | pubmed:abstractText | Small molecule inhibitors provide powerful tools to characterize highly dynamic and complex eukaryotic cell pathways such as those mediating membrane traffic. However, a lack of easy and generalizable assays has constrained identification of novel inhibitors despite availability of diverse chemical libraries. Here, we report a facile growth-based strategy in yeast to screen for pathway-specific inhibitors. The approach uses well characterized synthetic genetic growth defects to guide design of cells genetically sensitized for inhibition of chosen pathways. With this strategy, we identified a family of piperazinyl phenylethanone compounds as inhibitors of traffic between the trans-Golgi network (TGN) and endosomes that depends on the clathrin adaptor complex AP-1. The compounds did not significantly alter other trafficking pathways involving the TGN or endosomes, indicating specificity. Compound treatment also altered localization of AP-1 in mammalian cells. These previously uncharacterized inhibitors will be useful for future studies of clathrin-mediated transport in yeast, and potentially in other organisms. Furthermore, the easily automated technology should be adaptable for identification of inhibitors of other cellular processes. | lld:pubmed |
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| pubmed-article:17404221 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17404221 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17404221 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17404221 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17404221 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17404221 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:17404221 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:17404221 | pubmed:author | pubmed-author:HuangJingJ | lld:pubmed |
| pubmed-article:17404221 | pubmed:author | pubmed-author:PayneGregory... | lld:pubmed |
| pubmed-article:17404221 | pubmed:author | pubmed-author:JungMichael... | lld:pubmed |
| pubmed-article:17404221 | pubmed:author | pubmed-author:HoDavid GDG | lld:pubmed |
| pubmed-article:17404221 | pubmed:author | pubmed-author:DuncanMara... | lld:pubmed |
| pubmed-article:17404221 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17404221 | pubmed:day | 10 | lld:pubmed |
| pubmed-article:17404221 | pubmed:volume | 104 | lld:pubmed |
| pubmed-article:17404221 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17404221 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17404221 | pubmed:pagination | 6235-40 | lld:pubmed |
| pubmed-article:17404221 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:17404221 | pubmed:meshHeading | pubmed-meshheading:17404221... | lld:pubmed |
| pubmed-article:17404221 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17404221 | pubmed:articleTitle | Composite synthetic lethal identification of membrane traffic inhibitors. | lld:pubmed |
| pubmed-article:17404221 | pubmed:affiliation | Department of Biological Chemistry, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA. | lld:pubmed |
| pubmed-article:17404221 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17404221 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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