pubmed-article:12960419 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12960419 | lifeskim:mentions | umls-concept:C0014239 | lld:lifeskim |
pubmed-article:12960419 | lifeskim:mentions | umls-concept:C0018042 | lld:lifeskim |
pubmed-article:12960419 | lifeskim:mentions | umls-concept:C0598953 | lld:lifeskim |
pubmed-article:12960419 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
pubmed-article:12960419 | pubmed:issue | 12 | lld:pubmed |
pubmed-article:12960419 | pubmed:dateCreated | 2003-11-25 | lld:pubmed |
pubmed-article:12960419 | pubmed:abstractText | Neo1p from Saccharomyces cerevisiae is an essential P-type ATPase and potential aminophospholipid translocase (flippase) in the Drs2p family. We have previously implicated Drs2p in protein transport steps in the late secretory pathway requiring ADP-ribosylation factor (ARF) and clathrin. Here, we present evidence that epitope-tagged Neo1p localizes to the endoplasmic reticulum (ER) and Golgi complex and is required for a retrograde transport pathway between these organelles. Using conditional alleles of NEO1, we find that loss of Neo1p function causes cargo-specific defects in anterograde protein transport early in the secretory pathway and perturbs glycosylation in the Golgi complex. Rer1-GFP, a protein that cycles between the ER and Golgi complex in COPI and COPII vesicles, is mislocalized to the vacuole in neo1-ts at the nonpermissive temperature. These phenotypes suggest that the anterograde protein transport defect is a secondary consequence of a defect in a COPI-dependent retrograde pathway. We propose that loss of lipid asymmetry in the cis Golgi perturbs retrograde protein transport to the ER. | lld:pubmed |
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pubmed-article:12960419 | pubmed:language | eng | lld:pubmed |
pubmed-article:12960419 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12960419 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12960419 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12960419 | pubmed:month | Dec | lld:pubmed |
pubmed-article:12960419 | pubmed:issn | 1059-1524 | lld:pubmed |
pubmed-article:12960419 | pubmed:author | pubmed-author:HuaZhaolinZ | lld:pubmed |
pubmed-article:12960419 | pubmed:author | pubmed-author:GrahamTodd... | lld:pubmed |
pubmed-article:12960419 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12960419 | pubmed:volume | 14 | lld:pubmed |
pubmed-article:12960419 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12960419 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12960419 | pubmed:pagination | 4971-83 | lld:pubmed |
pubmed-article:12960419 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:12960419 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12960419 | pubmed:articleTitle | Requirement for neo1p in retrograde transport from the Golgi complex to the endoplasmic reticulum. | lld:pubmed |
pubmed-article:12960419 | pubmed:affiliation | Department of Biological Sciences, Vanderbilt University, Nashville, Tennessee 37235-1634, USA. | lld:pubmed |
pubmed-article:12960419 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12960419 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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