| pubmed-article:14617738 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14617738 | lifeskim:mentions | umls-concept:C0237401 | lld:lifeskim |
| pubmed-article:14617738 | lifeskim:mentions | umls-concept:C0020792 | lld:lifeskim |
| pubmed-article:14617738 | lifeskim:mentions | umls-concept:C1412111 | lld:lifeskim |
| pubmed-article:14617738 | lifeskim:mentions | umls-concept:C1420304 | lld:lifeskim |
| pubmed-article:14617738 | lifeskim:mentions | umls-concept:C0016315 | lld:lifeskim |
| pubmed-article:14617738 | lifeskim:mentions | umls-concept:C1510438 | lld:lifeskim |
| pubmed-article:14617738 | lifeskim:mentions | umls-concept:C0243077 | lld:lifeskim |
| pubmed-article:14617738 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:14617738 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:14617738 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:14617738 | pubmed:dateCreated | 2004-2-10 | lld:pubmed |
| pubmed-article:14617738 | pubmed:abstractText | Acyl CoA:cholesterol acyltransferase 1 (ACAT1) and ACAT2 are enzymes responsible for the formation of cholesteryl esters in tissues. While both ACAT1 and ACAT2 are present in the liver and intestine, the cells containing either enzyme within these tissues are distinct, suggesting that ACAT1 and ACAT2 have separate functions. In this study, NBD-cholesterol was used to screen for specific inhibitors of ACAT1 and ACAT2. Incubation of AC29 cells, which do not contain ACAT activity, with NBD-cholesterol showed weak fluorescence when the compound was localized in the membrane. When AC29 cells stably transfected with either ACAT1 or ACAT2 were incubated with NBD-cholesterol, the fluorescent signal localized to the nonpolar core of cytoplasmic lipid droplets was strongly fluorescent and was correlated with two independent measures of ACAT activity. Several compounds were found to have greater inhibitory activity toward ACAT1 than ACAT2, and one compound was identified that specifically inhibits ACAT2. The demonstration of selective inhibition of ACAT1 and ACAT2 provides evidence for uniqueness in structure and function of these two enzymes. To the extent that ACAT2 is confined to hepatocytes and enterocytes, the only two cell types that secrete lipoproteins, selective inhibition of ACAT2 may prove to be most beneficial in the reduction of plasma lipoprotein cholesterol concentrations. | lld:pubmed |
| pubmed-article:14617738 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14617738 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:14617738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14617738 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14617738 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:14617738 | pubmed:issn | 0022-2275 | lld:pubmed |
| pubmed-article:14617738 | pubmed:author | pubmed-author:OmuraSatoshiS | lld:pubmed |
| pubmed-article:14617738 | pubmed:author | pubmed-author:RudelLawrence... | lld:pubmed |
| pubmed-article:14617738 | pubmed:author | pubmed-author:LadaAaron TAT | lld:pubmed |
| pubmed-article:14617738 | pubmed:author | pubmed-author:TomodaHiroshi... | lld:pubmed |
| pubmed-article:14617738 | pubmed:author | pubmed-author:DavisMatthewM | lld:pubmed |
| pubmed-article:14617738 | pubmed:author | pubmed-author:KentCarolC | lld:pubmed |
| pubmed-article:14617738 | pubmed:author | pubmed-author:ChapmanJamesJ | lld:pubmed |
| pubmed-article:14617738 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14617738 | pubmed:volume | 45 | lld:pubmed |
| pubmed-article:14617738 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14617738 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14617738 | pubmed:pagination | 378-86 | lld:pubmed |
| pubmed-article:14617738 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:meshHeading | pubmed-meshheading:14617738... | lld:pubmed |
| pubmed-article:14617738 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:14617738 | pubmed:articleTitle | Identification of ACAT1- and ACAT2-specific inhibitors using a novel, cell-based fluorescence assay: individual ACAT uniqueness. | lld:pubmed |
| pubmed-article:14617738 | pubmed:affiliation | Department of Pathology, Arteriosclerosis Research Program, Wake Forest University School of Medicine, Winston-Salem, NC, USA. | lld:pubmed |
| pubmed-article:14617738 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14617738 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:14617738 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:14617738 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:14617738 | lld:pubmed |
