Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2010-4-14
pubmed:abstractText
The liver X receptors LXRalpha and LXRbeta play critical roles in maintaining lipid homeostasis by functioning as transcription factors that regulate genetic networks controlling the transport, catabolism, and excretion of cholesterol. The studies described in this report examine the individual anti-atherogenic activity of LXRalpha and LXRbeta and determine the ability of each subtype to mediate the biological response to LXR agonists. Utilizing individual knockouts of LXRalpha and LXRbeta in the Ldlr(-/-) background, we demonstrate that LXRalpha has a dominant role in limiting atherosclerosis in vivo. Functional studies in macrophages indicate that LXRalpha is required for a robust response to LXR ligands, whereas LXRbeta functions more strongly as a repressor. Furthermore, selective knockout of LXRalpha in hematopoietic cells and rescue experiments indicate that the anti-atherogenic activity of this LXR subtype is not restricted to macrophages. These studies indicate that LXRalpha plays a selective role in limiting atherosclerosis in response to hyperlipidemia.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-10858438, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-10968783, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-11090130, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-11090131, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-11149950, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-11239408, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-12032330, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-12193651, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-12196343, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-12586329, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-12601003, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-12690094, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-12897148, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-15539622, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-16024916, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-16325781, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-16511593, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-16825483, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-17556891, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-17657314, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-17720994, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-18096827, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-18614014, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-18650918, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-18787185, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-18974038, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-8656070, http://linkedlifedata.com/resource/pubmed/commentcorrection/20388921-9630215
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-2275
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
900-6
pubmed:dateRevised
2011-7-28
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Non-redundant roles for LXRalpha and LXRbeta in atherosclerosis susceptibility in low density lipoprotein receptor knockout mice.
pubmed:affiliation
Exelixis, Inc., San Diego, CA, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural