| pubmed-article:10359606 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10359606 | lifeskim:mentions | umls-concept:C0043393 | lld:lifeskim |
| pubmed-article:10359606 | lifeskim:mentions | umls-concept:C0682323 | lld:lifeskim |
| pubmed-article:10359606 | lifeskim:mentions | umls-concept:C1413246 | lld:lifeskim |
| pubmed-article:10359606 | lifeskim:mentions | umls-concept:C1826471 | lld:lifeskim |
| pubmed-article:10359606 | lifeskim:mentions | umls-concept:C1837441 | lld:lifeskim |
| pubmed-article:10359606 | lifeskim:mentions | umls-concept:C0439855 | lld:lifeskim |
| pubmed-article:10359606 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:10359606 | pubmed:dateCreated | 1999-7-29 | lld:pubmed |
| pubmed-article:10359606 | pubmed:abstractText | Six new members of the yeast p24 family have been identified and characterized. These six genes, named ERP1-ERP6 (for Emp24p- and Erv25p-related proteins) are not essential, but deletion of ERP1 or ERP2 causes defects in the transport of Gas1p, in the retention of BiP, and deletion of ERP1 results in the suppression of a temperature-sensitive mutation in SEC13 encoding a COPII vesicle coat protein. These phenotypes are similar to those caused by deletion of EMP24 or ERV25, two previously identified genes that encode related p24 proteins. Genetic and biochemical studies demonstrate that Erp1p and Erp2p function in a heteromeric complex with Emp24p and Erv25p. | lld:pubmed |
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| pubmed-article:10359606 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10359606 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10359606 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10359606 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:10359606 | pubmed:issn | 1059-1524 | lld:pubmed |
| pubmed-article:10359606 | pubmed:author | pubmed-author:WilsonRR | lld:pubmed |
| pubmed-article:10359606 | pubmed:author | pubmed-author:ThomasD YDY | lld:pubmed |
| pubmed-article:10359606 | pubmed:author | pubmed-author:BergeronJ JJJ | lld:pubmed |
| pubmed-article:10359606 | pubmed:author | pubmed-author:HerrmannJ MJM | lld:pubmed |
| pubmed-article:10359606 | pubmed:author | pubmed-author:RowlesGG | lld:pubmed |
| pubmed-article:10359606 | pubmed:author | pubmed-author:MarziochMM | lld:pubmed |
| pubmed-article:10359606 | pubmed:author | pubmed-author:SolariR CRC | lld:pubmed |
| pubmed-article:10359606 | pubmed:author | pubmed-author:HenthornD CDC | lld:pubmed |
| pubmed-article:10359606 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10359606 | pubmed:volume | 10 | lld:pubmed |
| pubmed-article:10359606 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10359606 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10359606 | pubmed:pagination | 1923-38 | lld:pubmed |
| pubmed-article:10359606 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10359606 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10359606 | pubmed:articleTitle | Erp1p and Erp2p, partners for Emp24p and Erv25p in a yeast p24 complex. | lld:pubmed |
| pubmed-article:10359606 | pubmed:affiliation | Cell Biology Unit, Glaxo-Wellcome Research and Development, Stevenage, Hertfordshire, SG1 2NY, United Kingdom. | lld:pubmed |
| pubmed-article:10359606 | pubmed:publicationType | Journal Article | lld:pubmed |
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