LXR regulates cholesterol uptake through Idol-dependent ubiquitination of the LDL receptor

Cellular cholesterol levels reflect a balance between uptake, efflux, and endogenous synthesis. Here we show that the sterol-responsive nuclear liver X receptor (LXR) helps maintain cholesterol homeostasis, not only through promotion of cholesterol efflux but also through suppression of low-density...

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Veröffentlicht in:Science (American Association for the Advancement of Science) Jg. 325; H. 5936; S. 100
Hauptverfasser: Zelcer, Noam, Hong, Cynthia, Boyadjian, Rima, Tontonoz, Peter
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 03.07.2009
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ISSN:1095-9203, 1095-9203
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Abstract Cellular cholesterol levels reflect a balance between uptake, efflux, and endogenous synthesis. Here we show that the sterol-responsive nuclear liver X receptor (LXR) helps maintain cholesterol homeostasis, not only through promotion of cholesterol efflux but also through suppression of low-density lipoprotein (LDL) uptake. LXR inhibits the LDL receptor (LDLR) pathway through transcriptional induction of Idol (inducible degrader of the LDLR), an E3 ubiquitin ligase that triggers ubiquitination of the LDLR on its cytoplasmic domain, thereby targeting it for degradation. LXR ligand reduces, whereas LXR knockout increases, LDLR protein levels in vivo in a tissue-selective manner. Idol knockdown in hepatocytes increases LDLR protein levels and promotes LDL uptake. Conversely, adenovirus-mediated expression of Idol in mouse liver promotes LDLR degradation and elevates plasma LDL levels. The LXR-Idol-LDLR axis defines a complementary pathway to sterol response element-binding proteins for sterol regulation of cholesterol uptake.
AbstractList Cellular cholesterol levels reflect a balance between uptake, efflux, and endogenous synthesis. Here we show that the sterol-responsive nuclear liver X receptor (LXR) helps maintain cholesterol homeostasis, not only through promotion of cholesterol efflux but also through suppression of low-density lipoprotein (LDL) uptake. LXR inhibits the LDL receptor (LDLR) pathway through transcriptional induction of Idol (inducible degrader of the LDLR), an E3 ubiquitin ligase that triggers ubiquitination of the LDLR on its cytoplasmic domain, thereby targeting it for degradation. LXR ligand reduces, whereas LXR knockout increases, LDLR protein levels in vivo in a tissue-selective manner. Idol knockdown in hepatocytes increases LDLR protein levels and promotes LDL uptake. Conversely, adenovirus-mediated expression of Idol in mouse liver promotes LDLR degradation and elevates plasma LDL levels. The LXR-Idol-LDLR axis defines a complementary pathway to sterol response element-binding proteins for sterol regulation of cholesterol uptake.
Cellular cholesterol levels reflect a balance between uptake, efflux, and endogenous synthesis. Here we show that the sterol-responsive nuclear liver X receptor (LXR) helps maintain cholesterol homeostasis, not only through promotion of cholesterol efflux but also through suppression of low-density lipoprotein (LDL) uptake. LXR inhibits the LDL receptor (LDLR) pathway through transcriptional induction of Idol (inducible degrader of the LDLR), an E3 ubiquitin ligase that triggers ubiquitination of the LDLR on its cytoplasmic domain, thereby targeting it for degradation. LXR ligand reduces, whereas LXR knockout increases, LDLR protein levels in vivo in a tissue-selective manner. Idol knockdown in hepatocytes increases LDLR protein levels and promotes LDL uptake. Conversely, adenovirus-mediated expression of Idol in mouse liver promotes LDLR degradation and elevates plasma LDL levels. The LXR-Idol-LDLR axis defines a complementary pathway to sterol response element-binding proteins for sterol regulation of cholesterol uptake.Cellular cholesterol levels reflect a balance between uptake, efflux, and endogenous synthesis. Here we show that the sterol-responsive nuclear liver X receptor (LXR) helps maintain cholesterol homeostasis, not only through promotion of cholesterol efflux but also through suppression of low-density lipoprotein (LDL) uptake. LXR inhibits the LDL receptor (LDLR) pathway through transcriptional induction of Idol (inducible degrader of the LDLR), an E3 ubiquitin ligase that triggers ubiquitination of the LDLR on its cytoplasmic domain, thereby targeting it for degradation. LXR ligand reduces, whereas LXR knockout increases, LDLR protein levels in vivo in a tissue-selective manner. Idol knockdown in hepatocytes increases LDLR protein levels and promotes LDL uptake. Conversely, adenovirus-mediated expression of Idol in mouse liver promotes LDLR degradation and elevates plasma LDL levels. The LXR-Idol-LDLR axis defines a complementary pathway to sterol response element-binding proteins for sterol regulation of cholesterol uptake.
Author Tontonoz, Peter
Boyadjian, Rima
Hong, Cynthia
Zelcer, Noam
Author_xml – sequence: 1
  givenname: Noam
  surname: Zelcer
  fullname: Zelcer, Noam
  organization: Howard Hughes Medical Institute and Department of Pathology and Laboratory Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA
– sequence: 2
  givenname: Cynthia
  surname: Hong
  fullname: Hong, Cynthia
– sequence: 3
  givenname: Rima
  surname: Boyadjian
  fullname: Boyadjian, Rima
– sequence: 4
  givenname: Peter
  surname: Tontonoz
  fullname: Tontonoz, Peter
BackLink https://www.ncbi.nlm.nih.gov/pubmed/19520913$$D View this record in MEDLINE/PubMed
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Snippet Cellular cholesterol levels reflect a balance between uptake, efflux, and endogenous synthesis. Here we show that the sterol-responsive nuclear liver X...
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SubjectTerms Animals
Cell Line, Tumor
Cholesterol - metabolism
DNA-Binding Proteins - agonists
DNA-Binding Proteins - metabolism
Homeostasis
Humans
Ligands
Lipoproteins, LDL - blood
Lipoproteins, LDL - metabolism
Liver - metabolism
Liver X Receptors
Mice
Mice, Inbred C57BL
Orphan Nuclear Receptors
Promoter Regions, Genetic
Receptors, Cytoplasmic and Nuclear - agonists
Receptors, Cytoplasmic and Nuclear - metabolism
Receptors, LDL - genetics
Receptors, LDL - metabolism
RNA, Messenger - genetics
RNA, Messenger - metabolism
Transcription, Genetic
Ubiquitin-Protein Ligases
Ubiquitination
Title LXR regulates cholesterol uptake through Idol-dependent ubiquitination of the LDL receptor
URI https://www.ncbi.nlm.nih.gov/pubmed/19520913
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