pubmed-article:14573790 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:14573790 | lifeskim:mentions | umls-concept:C0026237 | lld:lifeskim |
pubmed-article:14573790 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
pubmed-article:14573790 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:14573790 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:14573790 | lifeskim:mentions | umls-concept:C1424327 | lld:lifeskim |
pubmed-article:14573790 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:14573790 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:14573790 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
pubmed-article:14573790 | lifeskim:mentions | umls-concept:C1516044 | lld:lifeskim |
pubmed-article:14573790 | pubmed:issue | 12 | lld:pubmed |
pubmed-article:14573790 | pubmed:dateCreated | 2003-10-23 | lld:pubmed |
pubmed-article:14573790 | pubmed:abstractText | Phospholipid scramblase 3 (PLS3) is a newly recognized member of a family of proteins responsible for phospholipid translocation between two lipid compartments. To study PLS3 function in mitochondria, we disrupted its conserved calcium-binding motif yielding an inactive mutant PLS3(F258V). Cells transfected with PLS3(F258V) exhibited reduced proliferative capacity. Mitochondrial analysis revealed that PLS3(F258V)-expressing cells have decreased mitochondrial mass shown by lower cytochrome c and cardiolipin (CL) content, poor mitochondrial respiration, and reduced oxygen consumption and intracellular ATP; whereas wild-type PLS3-transfected cells exhibit increased mitochondrial mass and enhanced respiration. Electron microscopic examination revealed that the mitochondria in PLS3(F258V)-expressing cells have densely packed cristae and are fewer in number and larger than those in control cells. The abnormal mitochondrial metabolism and structure in PLS3(F258V)-expressing cells were associated with decreased sensitivity to UV- and tBid-induced apoptosis and diminished translocation of CL to the mitochondrial outer membrane. In contrast, wild-type PLS3-transfected cells displayed increased sensitivity to apoptosis and enhanced CL translocation. These studies identify PLS3 as a critical regulator of mitochondrial structure and respiration, and CL transport in apoptosis. | lld:pubmed |
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pubmed-article:14573790 | pubmed:language | eng | lld:pubmed |
pubmed-article:14573790 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14573790 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:14573790 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:14573790 | pubmed:month | Oct | lld:pubmed |
pubmed-article:14573790 | pubmed:issn | 1541-7786 | lld:pubmed |
pubmed-article:14573790 | pubmed:author | pubmed-author:TurkD RDR | lld:pubmed |
pubmed-article:14573790 | pubmed:author | pubmed-author:ChenJunJ | lld:pubmed |
pubmed-article:14573790 | pubmed:author | pubmed-author:LiuJihuaJ | lld:pubmed |
pubmed-article:14573790 | pubmed:author | pubmed-author:GrossmanDougl... | lld:pubmed |
pubmed-article:14573790 | pubmed:author | pubmed-author:FreemanAngela... | lld:pubmed |
pubmed-article:14573790 | pubmed:author | pubmed-author:DaiQiangQ | lld:pubmed |
pubmed-article:14573790 | pubmed:author | pubmed-author:LeeRay MRM | lld:pubmed |
pubmed-article:14573790 | pubmed:author | pubmed-author:DurrantDavidD | lld:pubmed |
pubmed-article:14573790 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:14573790 | pubmed:volume | 1 | lld:pubmed |
pubmed-article:14573790 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:14573790 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:14573790 | pubmed:pagination | 892-902 | lld:pubmed |
pubmed-article:14573790 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:14573790 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:14573790 | pubmed:articleTitle | Phospholipid scramblase 3 controls mitochondrial structure, function, and apoptotic response. | lld:pubmed |
pubmed-article:14573790 | pubmed:affiliation | Huntsman Cancer Institute,, University of Utah, Salt Lake City, UT 84112, USA. | lld:pubmed |
pubmed-article:14573790 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:14573790 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:14573790 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:14573790 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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