pubmed-article:8753648 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:8753648 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
pubmed-article:8753648 | lifeskim:mentions | umls-concept:C0949610 | lld:lifeskim |
pubmed-article:8753648 | lifeskim:mentions | umls-concept:C1424693 | lld:lifeskim |
pubmed-article:8753648 | lifeskim:mentions | umls-concept:C1706178 | lld:lifeskim |
pubmed-article:8753648 | lifeskim:mentions | umls-concept:C1336669 | lld:lifeskim |
pubmed-article:8753648 | lifeskim:mentions | umls-concept:C1840423 | lld:lifeskim |
pubmed-article:8753648 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:8753648 | pubmed:dateCreated | 1996-11-5 | lld:pubmed |
pubmed-article:8753648 | pubmed:abstractText | The AFG3 gene of Saccharomyces cerevisiae encodes a mitochondrial inner membrane protein with ATP-dependent protease activity. To gain more insight into the function of this protein, multi-copy suppressors of an afg3-null mutation were isolated. Three genes were found that restored partial growth on non-fermentable carbon sources, all of which affect the biogenesis of respiratory competent mitochondria: PIM1(LON) encodes a matrix-localized ATP-dependent protease involved in the turnover of matrix proteins; OXA1(PET1402) encodes a putative mitochondrial inner membrane protein involved in the biogenesis of the respiratory chain; and MBA1 encodes a mitochondrial protein required for optimal respiratory growth. All three genes also suppressed a null mutation in a related gene, RCA1, as well as in the combination of afg3- and rca1-null. | lld:pubmed |
pubmed-article:8753648 | pubmed:language | eng | lld:pubmed |
pubmed-article:8753648 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:8753648 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:8753648 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:8753648 | pubmed:month | Aug | lld:pubmed |
pubmed-article:8753648 | pubmed:issn | 0172-8083 | lld:pubmed |
pubmed-article:8753648 | pubmed:author | pubmed-author:LeggR FRF | lld:pubmed |
pubmed-article:8753648 | pubmed:author | pubmed-author:RehEE | lld:pubmed |
pubmed-article:8753648 | pubmed:author | pubmed-author:GrivellL ALA | lld:pubmed |
pubmed-article:8753648 | pubmed:author | pubmed-author:GuélinEE | lld:pubmed |
pubmed-article:8753648 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:8753648 | pubmed:volume | 30 | lld:pubmed |
pubmed-article:8753648 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:8753648 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:8753648 | pubmed:pagination | 206-11 | lld:pubmed |
pubmed-article:8753648 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:8753648 | pubmed:year | 1996 | lld:pubmed |
pubmed-article:8753648 | pubmed:articleTitle | Three genes for mitochondrial proteins suppress null-mutations in both Afg3 and Rca1 when over-expressed. | lld:pubmed |
pubmed-article:8753648 | pubmed:affiliation | Department of Molecular Cell Biology, University of Amsterdam, Kruislaan 318, 1098 SM Amsterdam, The Netherlands. | lld:pubmed |
pubmed-article:8753648 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:8753648 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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