rdf:type |
|
lifeskim:mentions |
umls-concept:C0011155,
umls-concept:C0017262,
umls-concept:C0023821,
umls-concept:C0024432,
umls-concept:C0026809,
umls-concept:C0162638,
umls-concept:C0185117,
umls-concept:C0332281,
umls-concept:C0392756,
umls-concept:C0524828,
umls-concept:C1121571,
umls-concept:C1413218,
umls-concept:C1517945,
umls-concept:C2911684
|
pubmed:issue |
1
|
pubmed:dateCreated |
2010-7-12
|
pubmed:abstractText |
Paraoxonase 1 (PON1) was shown to stimulate HDL binding and HDL-mediated cholesterol efflux from macrophages. This study examined the role of PON1 in the expression of proteins that enhance macrophage HDL binding, i.e. ABCA1 and SR-BI.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jul
|
pubmed:issn |
1879-1484
|
pubmed:author |
|
pubmed:copyrightInfo |
Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.
|
pubmed:issnType |
Electronic
|
pubmed:volume |
211
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
61-8
|
pubmed:meshHeading |
pubmed-meshheading:20149374-Animals,
pubmed-meshheading:20149374-Apoptosis,
pubmed-meshheading:20149374-Aryldialkylphosphatase,
pubmed-meshheading:20149374-Cell Line,
pubmed-meshheading:20149374-Humans,
pubmed-meshheading:20149374-Lipoproteins, HDL,
pubmed-meshheading:20149374-Lysophosphatidylcholines,
pubmed-meshheading:20149374-Macrophages,
pubmed-meshheading:20149374-Mice,
pubmed-meshheading:20149374-Mice, Inbred C57BL,
pubmed-meshheading:20149374-Scavenger Receptors, Class B,
pubmed-meshheading:20149374-Up-Regulation
|
pubmed:year |
2010
|
pubmed:articleTitle |
Paraoxonase 1 (PON1) deficiency in mice is associated with reduced expression of macrophage SR-BI and consequently the loss of HDL cytoprotection against apoptosis.
|
pubmed:affiliation |
The Lipid Research Laboratory, Technion Faculty of Medicine, The Rappaport Family Institute for Research in the Medical Sciences, and Rambam Medical Center, 31096 Haifa, Israel. Fuhrman@tx.technion.ac.il
|
pubmed:publicationType |
Journal Article
|