pubmed-article:17881569 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17881569 | lifeskim:mentions | umls-concept:C0018042 | lld:lifeskim |
pubmed-article:17881569 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
pubmed-article:17881569 | lifeskim:mentions | umls-concept:C0069838 | lld:lifeskim |
pubmed-article:17881569 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:17881569 | pubmed:issue | 39 | lld:pubmed |
pubmed-article:17881569 | pubmed:dateCreated | 2007-9-26 | lld:pubmed |
pubmed-article:17881569 | pubmed:abstractText | The Saccharomyces cerevisiae phosphatidylcholine/phosphatidylinositol transfer protein Sec14p is required for Golgi apparatus-derived vesicular transport through coordinate regulation of phospholipid metabolism. Sec14p is normally essential. The essential requirement for SEC14 can be bypassed by inactivation of (i) the CDP-choline pathway for phosphatidylcholine synthesis or (ii) KES1, which encodes an oxysterol binding protein. A unique screen was used to determine genome-wide genetic interactions for the essential gene SEC14 and to assess whether the two modes of "sec14 bypass" were similar or distinct. The results indicate that inactivation of the CDP-choline pathway allows cells with inactivated SEC14 to live through a mechanism distinct from that of inactivation of KES1. We go on to demonstrate an important biological function of Kes1p. Kes1p regulates Golgi apparatus-derived vesicular transport by inhibiting the function of Pik1p-generated Golgi apparatus phosphatidylinositol-4-phosphate (PI-4P). Kes1p affects both the availability and level of Golgi apparatus PI-4P. A set of potential PI-4P-responsive proteins that include the Rab GTPase Ypt31p and its GTP exchange factor are described. | lld:pubmed |
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pubmed-article:17881569 | pubmed:language | eng | lld:pubmed |
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pubmed-article:17881569 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17881569 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17881569 | pubmed:month | Sep | lld:pubmed |
pubmed-article:17881569 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:17881569 | pubmed:author | pubmed-author:StefanChristo... | lld:pubmed |
pubmed-article:17881569 | pubmed:author | pubmed-author:McMasterChris... | lld:pubmed |
pubmed-article:17881569 | pubmed:author | pubmed-author:FairnGregory... | lld:pubmed |
pubmed-article:17881569 | pubmed:author | pubmed-author:CurwinAmy JAJ | lld:pubmed |
pubmed-article:17881569 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17881569 | pubmed:day | 25 | lld:pubmed |
pubmed-article:17881569 | pubmed:volume | 104 | lld:pubmed |
pubmed-article:17881569 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17881569 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17881569 | pubmed:pagination | 15352-7 | lld:pubmed |
pubmed-article:17881569 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:17881569 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17881569 | pubmed:articleTitle | The oxysterol binding protein Kes1p regulates Golgi apparatus phosphatidylinositol-4-phosphate function. | lld:pubmed |
pubmed-article:17881569 | pubmed:affiliation | Department of Pediatrics, Dalhousie University, Halifax, NS, Canada B3H 4H7. | lld:pubmed |
pubmed-article:17881569 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17881569 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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