The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index; 10 of the 11 sources its claims cite were checked for support.
Feedback Regulation of Cholesterol Uptake by the LXR–IDOL–LDLR Axis
Open accessAbstract
Inducible degrader of the low-density lipoprotein receptor (IDOL) is an E3 ubiquitin ligase that mediates the ubiquitination and degradation of the low-density lipoprotein receptor (LDLR). IDOL expression is controlled at the transcriptional level by the cholesterol-sensing nuclear receptor liver X receptor (LXR). In response to rising cellular sterol levels, activated LXR induces IDOL production, thereby limiting further uptake of exogenous cholesterol through the LDLR pathway. The LXR–IDOL–LDLR mechanism for feedback inhibition of cholesterol uptake is independent of and complementary to the sterol regulatory element–binding protein pathway. Since the initial description of the LXR–IDOL pathway, biochemical studies have helped to define the structural basis for both IDOL target recognition and LDLR ubiquitin transfer. Recent work has also suggested links between IDOL and human lipid metabolism.
Overview
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Written from the paper’s full text.
TL;DR
This review describes the LXR–IDOL–LDLR axis, in which LXR-induced IDOL ubiquitinates and degrades LDLR (and VLDLR/ApoER2), providing feedback inhibition of cholesterol uptake independent of SREBP. It synthesizes structural, cellular, mouse, and human genetic evidence and highlights unresolved questions about IDOL in human lipid metabolism.
Key findings
- IDOL is an E3 ubiquitin ligase whose promoter is directly regulated by LXR/RXR; LXR agonists induce IDOL and reduce LDLR protein without changing LDLR mRNA, and IDOL-null ES cells have higher basal LDLR protein and internalize LDL more readily. In IDOL-null ES cells, LXR agonists have no effect on LDLR protein or LDL uptake.
- The LXR–IDOL pathway acts acutely: oxysterol activation reduces plasma membrane LDLR protein in WT cells with a half-maximum effect as early as 2 h, whereas in IDOL-deficient cells LDLR downregulation is slower and only via SREBP-mediated transcriptional suppression.
- IDOL recognizes targets through its FERM F3b PTB-like domain binding a WxxKNxxSI/MxF motif in cytoplasmic tails; key LDLR residues include W813, I821, and F823, and IDOL residues Y265/T269 (with H272 implicated independently) are important. UBE2D family members (UBE2D1–4) support IDOL autoubiquitination and LDLR ubiquitination, while UBE2N/UBE2V1 has also been implicated.
- Human genetics: the N342S SNP in IDOL alters LDLR degradation (N342 more active than S342); in a cohort of Mexican hyperlipidemic patients, subjects homozygous for the less active S342 allele exhibited 7% lower plasma cholesterol. GWAS have linked IDOL-region SNPs to total cholesterol, LDL-cholesterol, and statin response.
Methods
- Narrative review; no new primary data are reported. It synthesizes published biochemical, cell-culture, mouse, structural, GWAS, and human cohort studies.
- Main analysis is qualitative integration of cited literature, including IDOL-deficient ES cells, LXR agonist treatments, adenoviral overexpression, mutagenesis, and in vitro ubiquitination assays.
- No systematic review methods, search strategy, or meta-analysis are reported.
Limitations
- Stated: the role of IDOL in human cholesterol metabolism remains an open question; no complete loss-of-function or dominant-negative IDOL alleles have been described, so effects of dramatic changes in IDOL activity are unknown, and whether pharmacologic inhibition of IDOL-dependent LDLR degradation would substantially affect human lipid levels is unknown.
- Stated: the relative importance of E2 enzymes (UBE2D vs UBE2N/UBE2V1) and of K48 vs K63 ubiquitin linkages in IDOL function remains to be clarified; the role of IDOL in brain development and function requires further study; and the mechanism for weaker IDOL responsiveness to LXR in mouse liver versus human hepatocyte cell lines is unknown.
- Evident: as a review, conclusions depend on previously published studies and no new experimental validation is presented.
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Claims the paper makes
9 Supported · 1 Partly supported · 1 No full text of the sources · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“In response to rising cellular sterol levels, activated LXR induces IDOL production, thereby limiting further uptake of exogenous cholesterol through the LDLR pathway.”
§ Feedback regulation of cholesterol uptake by the LXR-IDOL-LDLR axis > Abstract
What the sources say
- Supportedcites [5] Zelcer N Hong C Boyadjian R Tontonoz P Lxr regulates cholesterol uptake through idol-dependent ubiquitination of the ldl receptor. Science 2009 325 100 104 19520913 PMC2777523 source
The paper states that LXRs are activated in response to excess cellular cholesterol (passage 7) and that LXR induces Idol, which targets LDLR for degradation and limits LDL cholesterol uptake (passages 1–2). This supports the claimed sequence. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“These results provide in vivo evidence that modulating IDOL activity can affect the plasma LDL levels in humans.”
§ Feedback regulation of cholesterol uptake by the LXR-IDOL-LDLR axis > Involvement of IDOL in human cholesterol metabolism
What the sources say
- Supportedcites [43] Weissglas-Volkov D Calkin AC Tusie-Luna T Sinsheimer JS Zelcer N Riba L Tino AM Ordonez-Sanchez ML Cruz-Bautista I Aguilar-Salinas CA Tontonoz P Pajukanta P The n342s mylip polymorphism is associated with high total cholesterol and increased ldl receptor degradation in humans. J Clin Invest 2011 121 3062 3071 21765216 PMC3148733 source
The Abstract identifies MYLIP as IDOL and states that the findings suggest modulation of its activity can affect LDL-C levels. The Discussion links a MYLIP variant to changes in plasma cholesterol in Mexican individuals, supporting the claim's human in vivo context. (LLM, conf=0.91)
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Furthermore, in a cohort of Mexican hyperlipidemic patients, subjects homozygous for the less active S342 allele exhibited a 7% lower plasma cholesterol levels, a result that would be consistent with increased hepatic LDLR expression.43”
§ Feedback regulation of cholesterol uptake by the LXR-IDOL-LDLR axis > Involvement of IDOL in human cholesterol metabolism
What the sources say
- Partly supportedcites [43] Weissglas-Volkov D Calkin AC Tusie-Luna T Sinsheimer JS Zelcer N Riba L Tino AM Ordonez-Sanchez ML Cruz-Bautista I Aguilar-Salinas CA Tontonoz P Pajukanta P The n342s mylip polymorphism is associated with high total cholesterol and increased ldl receptor degradation in humans. J Clin Invest 2011 121 3062 3071 21765216 PMC3148733 sourceExperimental — accuracy not yet measured
The Association analysis section reports lower adjusted total cholesterol for Ser/Ser than Asn/Asn subjects in the Mexican dyslipidemic sample, and the Functional characterization section reports reduced LDLR degradation by S342. But the reported means are 5.20 versus 5.49 mmol/l—a difference of about 5.3%, not 7%. The Discussion predicts increased LDLR expression in vivo but says the contributions of specific tissues remain to be investigated. (LLM, conf=0.91)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Inducible Degrader Of the Low-density lipoprotein receptor (IDOL) is an E3 ubiquitin ligase that mediates the ubiquitination and degradation of the low-density lipoprotein receptor (LDLR).”
§ Feedback regulation of cholesterol uptake by the LXR-IDOL-LDLR axis > Abstract
What the sources say
- Supportedcites [5] Zelcer N Hong C Boyadjian R Tontonoz P Lxr regulates cholesterol uptake through idol-dependent ubiquitination of the ldl receptor. Science 2009 325 100 104 19520913 PMC2777523 source
The Abstract identifies Idol as an E3 ubiquitin ligase that triggers LDLR ubiquitination and targets it for degradation. The paper’s summary likewise states that Idol catalyzes LDLR ubiquitination, thereby targeting it for degradation. (LLM, conf=0.95)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“IDOL expression is controlled at the transcriptional level by the cholesterol-sensing nuclear receptor LXR.”
§ Feedback regulation of cholesterol uptake by the LXR-IDOL-LDLR axis > Abstract
What the sources say
- Supportedcites [5] Zelcer N Hong C Boyadjian R Tontonoz P Lxr regulates cholesterol uptake through idol-dependent ubiquitination of the ldl receptor. Science 2009 325 100 104 19520913 PMC2777523 source
The Abstract states that LXR suppresses LDL uptake through transcriptional induction of Idol and describes LXR as a sterol-responsive nuclear receptor. The passage on the Idol promoter further reports an LXR-responsive element and says the results suggest a direct transcriptional effect. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Through transcription profiling studies and candidate gene analyses, we identified the E3 ubiquitin ligase MYLIP (re-named IDOL) as the mediator of the effects of LXR on the LDLR.”
§ Feedback regulation of cholesterol uptake by the LXR-IDOL-LDLR axis > Regulation of IDOL expression by LXR
What the sources say
- Supportedcites [5] Zelcer N Hong C Boyadjian R Tontonoz P Lxr regulates cholesterol uptake through idol-dependent ubiquitination of the ldl receptor. Science 2009 325 100 104 19520913 PMC2777523 source
The paper’s Abstract identifies Mylip as the protein the authors propose renaming Idol and says they found it through transcriptional profiling of LXR target genes. It also states that LXR inhibits the LDLR pathway by inducing Idol, an E3 ubiquitin ligase that targets LDLR for degradation. The cited passages do not specifically describe a separate candidate-gene analysis, but they support the attributed identification and mechanism. (LLM, conf=0.95)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Treatment of various cell types including macrophages and hepatocytes with the LXR agonists GW3965 and T0901317 markedly inhibits the binding and uptake of LDL by these cells.5”
§ Feedback regulation of cholesterol uptake by the LXR-IDOL-LDLR axis > Regulation of IDOL expression by LXR
What the sources say
- Supportedcites [5] Zelcer N Hong C Boyadjian R Tontonoz P Lxr regulates cholesterol uptake through idol-dependent ubiquitination of the ldl receptor. Science 2009 325 100 104 19520913 PMC2777523 source
The passage describing Fig. 1A reports that LXR ligands decreased binding and uptake of labeled LDL in HepG2 human liver cells and primary mouse macrophages. It calls the ligands “GW3695 or T1317”; elsewhere the copy names GW3965. The reported cell types and effect match the claim. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
In the paper
“Indeed, we showed that the IDOL FERM domain binds directly to a recognition sequence in the cytoplasmic tails of its three known targets–LDLR, VLDLR, and ApoER2 (Figure 1).31”
§ Feedback regulation of cholesterol uptake by the LXR-IDOL-LDLR axis > The structural basis for substrate recognition by IDOL
What the sources say
- Not checked — no full text of the sourcecites [31] Calkin AC Goult BT Zhang L Fairall L Hong C Schwabe JW Tontonoz P Ferm-dependent e3 ligase recognition is a conserved mechanism for targeted degradation of lipoprotein receptors. Proc Natl Acad Sci U S A 2011 108 20107 20112 22109552 PMC3250164 source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 3
Every source the paper cites for this claim was checked and supports it.
In the paper
“Cells lacking IDOL expression exhibit higher basal levels of LDLR protein and internalize LDL more readily than wild-type cells.32”
- Also stated in: § Complementary regulation of the LDLR by the SREBP and the IDOL pathways · hedged
“Furthermore, synthetic LXR agonists have no effect on protein levels of the LDLR or the uptake of LDL in IDOL-null ES cells, indicating that IDOL is absolutely required for LXR's effect on the LDLR.32”
§ Feedback regulation of cholesterol uptake by the LXR-IDOL-LDLR axis > Complementary regulation of the LDLR by the SREBP and the IDOL pathways
What the sources say
- Supportedcites [32] Scotti E Hong C Yoshinaga Y Tu Y Hu Y Zelcer N Boyadjian R de Jong PJ Young SG Fong LG Tontonoz P Targeted disruption of the idol gene alters cellular regulation of the low-density lipoprotein receptor by sterols and liver x receptor agonists. Molecular and cellular biology 2011 31 1885 1893 21343340 PMC3133228 source
The Discussion states that Idol-null ES cells have much higher basal LDLR protein levels than wild-type cells and increased LDL uptake. It also reports that an LXR agonist did not affect LDLR protein expression or LDL uptake in those cells; the results accompanying Fig. 2 support both findings. (LLM, conf=0.95)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § Complementary regulation of the LDLR by the SREBP and the IDOL pathways · hedged
Every source the paper cites for this claim was checked and supports it.
In the paper
“The LXR–IDOL–LDLR mechanism for feedback inhibition of cholesterol uptake is independent of and complementary to the SREBP pathway.”
§ Feedback regulation of cholesterol uptake by the LXR-IDOL-LDLR axis > Abstract
What the sources say
- Supportedcites [32] Scotti E Hong C Yoshinaga Y Tu Y Hu Y Zelcer N Boyadjian R de Jong PJ Young SG Fong LG Tontonoz P Targeted disruption of the idol gene alters cellular regulation of the low-density lipoprotein receptor by sterols and liver x receptor agonists. Molecular and cellular biology 2011 31 1885 1893 21343340 PMC3133228 source
The Discussion describes Idol and SREBP-2 as complementary pathways in feedback control of LDLR protein levels by sterols. The paper also states that Idol and SREBP are independent but complementary mechanisms for LDLR regulation, and that Idol-mediated LDLR degradation limits cholesterol uptake. Page numbers are not supplied in our copy. (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Furthermore, PCSK9 is still able to stimulate LDLR degradation in cells lacking IDOL, indicating that IDOL and PCSK9 function in complementary but independent pathways.32”
§ Feedback regulation of cholesterol uptake by the LXR-IDOL-LDLR axis > Complementary regulation of the LDLR by the SREBP and the IDOL pathways
What the sources say
- Supportedcites [32] Scotti E Hong C Yoshinaga Y Tu Y Hu Y Zelcer N Boyadjian R de Jong PJ Young SG Fong LG Tontonoz P Targeted disruption of the idol gene alters cellular regulation of the low-density lipoprotein receptor by sterols and liver x receptor agonists. Molecular and cellular biology 2011 31 1885 1893 21343340 PMC3133228 source
The Discussion states that PCSK9 induces LDLR degradation in Idol-deficient cells and concludes that the two act in complementary but independent pathways. The ‘Relationship of Idol to the statin and PCSK9 pathways’ section reports the supporting experiment in embryonic stem cells. (LLM, conf=0.94)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“IDOL is a well-characterized transcriptional target of the liver X receptors (LXRs) (8, 32)”
From SUMOylation of the ubiquitin ligase IDOL decreases LDL receptor levels and is reversed by SENP1 (2021) · cites this paper as [32]
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Metadata
- Authors
- Zhang, L., Reue, K., Fong, L. G., Young, S. G., & Tontonoz, P.
- Affiliations
- Howard Hughes Medical Institute (US)
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2012-11
- Volume
- 32
- Issue
- 11
- Pages
- 2541-2546
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- PMC
- PMC4280256
- OpenAlex
- W2157159684
- Cited by
- 137
- References
- 44
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 19 · 2023: 7 · 2022: 13 · 2021: 10 · 2020: 11 · 2019: 5 · 2018: 7 · 2017: 4 · 2016: 18 · 2015: 11 · 2014: 9 · 2013: 11
- FWCI
- 1.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (HL090553)
- National Heart, Lung, and Blood Institute (P01HL090553, HL066088, R01HL066088)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- liver X receptor, idols, LDL receptor, cholesterol absorption, feedback regulation, E3 ubiquitin ligase, LDLR degradation, SREBP, cholesterol sensing, lipid metabolism, ubiquitination
- MeSH terms
- Liver X Receptors, Animals, Biological Transport, Cholesterol, Humans, Liver, Receptors, LDL, Substrate Specificity, Gene Expression Regulation, Enzymologic, Feedback, Physiological, Ubiquitin-Protein Ligases, Atherosclerosis, Ubiquitination, Orphan Nuclear Receptors
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