Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-6-12
pubmed:abstractText
Macrophage-derived apolipoprotein E (apoE) influences the susceptibility of the arterial wall to atherosclerosis. Previous studies have shown that production of apoE in these cells is regulated at a posttranscriptional level and is increased by inhibitors of proteasomal degradation. To further investigate this mechanism, we stably transfected RAW 264.7 macrophages and HepG2 cells with a construct overexpressing ubiquitin, the peptide targeting proteins to the proteasome, fused to an influenza virus hemagglutinin epitope tag. Ubiquitination of apoE was investigated by immunoprecipitation and Western blot analysis. In both cell types, apoE was ubiquitinated, and inhibition of proteasome function by lactacystin led to accumulation of ubiquitinated apoE. These studies provide strong evidence for proteasomal degradation of apoE in the two main cell types responsible for its production and indicate a possible new level of regulation of this important protein.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-291X
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
282
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
608-14
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Apolipoprotein E in macrophages and hepatocytes is eegraded via the proteasomal pathway.
pubmed:affiliation
Institute of Arteriosclerosis Research, University of Münster, Germany.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't