The DOI matches its Crossref record; 151 of the 151 references it cites were found in a registry or an index.
A Receptor-Mediated Pathway for Cholesterol Homeostasis
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In the citing paper
“LDLR is a receptor that binds to apolipoprotein B and apoE in the periphery to facilitate the uptake of cholesterol-laden lipoproteins by cells [38].”
From Measurement of apolipoprotein E and amyloid β clearance rates in the mouse brain using bolus stable isotope labeling (2012) · cites this paper as [38]
In the citing paper
“Ldlr is normally localized to the plasma membrane where it binds extracellular ApoE lipoproteins followed by endocytosis and subsequent release of bound lipids in the lysosome (62).”
From Regulation of astrocyte lipid metabolism and ApoE secretion by the microglial oxysterol, 25-hydroxycholesterol (2023) · cites this paper as [62]
In the citing paper
“LDLR is a cell surface glycoprotein that plays an important role in mediating the removal of cholesterol and cholesteryl ester-containing low-density lipoprotein (LDL) particles from the circulation (Brown and Goldstein, 1986; Herz and Bock, 2002).”
From The role of apolipoprotein E in Alzheimer's disease (2009) · cites this paper as Brown and Goldstein, 1986
In the citing paper
“LDL is catabolized by the liver via the LDL receptor (LDLR), which binds APOB and removes LDL from circulation and traffics it to the endosomal system for degradation (15).”
From Hepatic sortilin regulates both apolipoprotein B secretion and LDL catabolism (2012) · cites this paper as [15]
In the citing paper
“internalized LDL is released from LDLR in acidic compartments (29, 30)”
From The small GTPase RAB10 regulates endosomal recycling of the LDL receptor and transferrin receptor in hepatocytes (2022) · cites this paper as [30]
In the citing paper
“Cholesterol derived from low-density lipoprotein (LDL) is taken into cells through endocytosis mediated by LDL receptors (LDLRs) (1).”
From Last step in the path of LDL cholesterol from lysosome to plasma membrane to ER is governed by phosphatidylserine (2020) · cites this paper as [1]
In the citing paper
“LDL-derived cholesterol is taken up by LDLRs and released in lysosomes (1).”
From Last step in the path of LDL cholesterol from lysosome to plasma membrane to ER is governed by phosphatidylserine (2020) · cites this paper as [1]
In the citing paper
“A number of scholars reported that LDLR is a major determinant of circulating levels of LDL.[16][17][18]”
From USP16 Regulates the Stability and Function of LDL receptor by Deubiquitination (2020) · cites this paper as [18]
In the citing paper
“Upon binding of plasma LDLs, cell surface LDLRs are internalized and transported to endosomes, where low pH causes LDLR-LDL dissociation1.”
From Phosphatidylinositol-(4,5)-Bisphosphate Regulates Plasma Cholesterol Through LDL (Low-Density Lipoprotein) Receptor Lysosomal Degradation (2020) · cites this paper as [1]
In the citing paper
“As a transmembrane glycoprotein, low-density lipoprotein receptor (LDLR) is abundantly expressed on the surface of hepatocytes, where it facilitates the uptake of LDL cholesterol and maintains the homeostasis of lipid metabolism20,21.”
From ABCC4 impairs the clearance of plasma LDL cholesterol through suppressing LDLR expression in the liver (2025) · cites this paper as [21]
In the citing paper
“Low expression level of low-density lipoprotein receptor (LDLR) in hepatocytes leads to hypercholesterolemia and eventually contributes to atherosclerotic cardiovascular disease (ASCVD).”
From ABCC4 impairs the clearance of plasma LDL cholesterol through suppressing LDLR expression in the liver (2025) · cites this paper as [21]
In the citing paper
“Complete absence or defective LDLRs due to mutations in the LDLR gene cause FH, characterized by an autosomal dominant inheritance of hypercholesterolemia and premature ASCVD (a list of mutations can be found in Table 1)1–4.”
From Pathways and Molecular Mechanisms Governing LDL Receptor Regulation (2025) · cites this paper as [2]
In the citing paper
“where it is concentrated into clathrin-coated pits to internalize bound LDL by receptor-mediated endocytosis (discussed separately below)2”
From Pathways and Molecular Mechanisms Governing LDL Receptor Regulation (2025) · cites this paper as [2]
In the citing paper
“Low-density lipoprotein receptor (LDLR) is an integral membrane protein that is most abundantly expressed in the liver, where it binds to and removes LDL-C from the circulation by endocytosis4,5.”
From Triciribine increases LDLR expression and LDL uptake through stabilization of LDLR mRNA (2018) · cites this paper as [4]
In the citing paper
“Feedback suppression of SREBP2 pathway by LDLR plays a pivotal role in maintaining the balance of cholesterol levels between liver and blood (Brown and Goldstein, 1986).”
From GPR146 Deficiency Protects against Hypercholesterolemia and Atherosclerosis (2019) · cites this paper as Brown and Goldstein, 1986
In the citing paper
“hepatic cells also play major roles in removing LDL from the circulation”
From Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol (2016) · cites this paper as [7]
In the citing paper
“The main carriers of atherogenic circulating cholesterol in humans are the LDL particles, which are produced mainly by the liver to deliver cholesterol to peripheral tissues”
From Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol (2016) · cites this paper as [7]
In the citing paper
“The balance of serum cholesterol level is determined by dietary intake, synthesis, and catabolism”
From Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol (2016) · cites this paper as [7]
In the citing paper
“LDL clearance from the circulation by LDL receptor (LDLR)-mediated endocytosis by hepatic and peripheral tissues and subsequent feedback regulation of endogenous synthesis of cholesterol is a key determinant of serum LDL level”
From Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol (2016) · cites this paper as [7]
In the citing paper
“Excessive cholesterol in the circulation, upon uptake by the liver via LDL receptor (LDLR)-mediated endocytosis, suppresses endogenous synthesis of cholesterol in the liver”
From Endocytic adaptors Arh and Dab2 control homeostasis of circulatory cholesterol (2016) · cites this paper as [7]
In the citing paper
“The expression of liver LDL receptor (LDLR) regulates human plasma LDL-cholesterol (LDL-C) homeostasis”
From A novel posttranscriptional mechanism for dietary cholesterol-mediated suppression of liver LDL receptor expression (2014) · cites this paper as [2]
In the citing paper
“Following dissociation of the LDLR-LDL complex, LDL is directed to lysosomes whereas the LDLR recycles to the plasma membrane.”
From The LXR-IDOL axis defines a clathrin-, caveolae-, and dynamin-independent endocytic route for LDLR internalization and lysosomal degradation (2013) · cites this paper as [2]
In the citing paper
“Low density lipoprotein (LDL) cholesterol is taken up into cells via clathrin-mediated endocytosis of the LDL receptor (LDLR).”
From The LXR-IDOL axis defines a clathrin-, caveolae-, and dynamin-independent endocytic route for LDLR internalization and lysosomal degradation (2013) · cites this paper as [2]
In the citing paper
“LDL, which is derived by peripheral lipolysis of VLDL (very-low-density lipoprotein), is primarily cleared from the circulation in the liver via the LDLR (LDL receptor) pathway.1,2”
From (Pro)renin Receptor Inhibition Reprograms Hepatic Lipid Metabolism and Protects Mice From Diet-Induced Obesity and Hepatosteatosis (2018) · cites this paper as [1]
In the citing paper
“This results in induction of the full set of genes required for de novo biosynthesis of cholesterol via the mevalonate pathway and of the low-density lipoprotein receptor (LDLR) that is required for uptake of LDL-derived cholesterol (7,8).”
From A MARCH6 and IDOL E3 Ubiquitin Ligase Circuit Uncouples Cholesterol Synthesis from Lipoprotein Uptake in Hepatocytes (2016) · cites this paper as [8]
In the citing paper
“The LDLR structure from the N-terminus to the C-terminus includes seven ligand-binding domain repeats, an epidermal growth factor (EGF) precursor homology domain, an O-linked sugar domain, a transmembrane domain, and a cytoplasmic domain”
From ENO1–BACE2-mediated LDLR cleavage promotes liver cancer progression by remodelling cholesterol metabolism (2025) · cites this paper as Brown and Goldstein, 1986
In the citing paper
“Early studies on normal and FH fibroblasts demonstrated that LDLRs, shortly after being synthesized, appear on the cell surface where they gather in coated pits (1).”
In the citing paper
“The low density lipoprotein receptor (LDLR) 2 plays a pivotal role in the regulation of cholesterol metabolism (1).”
In the citing paper
“As noted in the Introduction, LDLR tends to cluster in clathrincoated pits on the cell surface under defined conditions.”
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Metadata
- Authors
- Brown, M. S., & Goldstein, J. L.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Venue
- Science
- Published
- 1986-04-04
- Volume
- 232
- Issue
- 4746
- Pages
- 34-47
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2084744450
- Semantic Scholar
- 272a968782c9511ffde67976c781969ead33e19e
- Cited by
- 5,703
- References
- 151
- Citations by year
- 2026: 64 · 2025: 78 · 2024: 61 · 2023: 105 · 2022: 107 · 2021: 125 · 2020: 118 · 2019: 108 · 2018: 131 · 2017: 140 · 2016: 130 · 2015: 145 · 2014: 139 · 2013: 134 · 2012: 139
- FWCI
- 30.50
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- cholesterol homeostasis, cholesterol metabolism, lipid transport
- MeSH terms
- Biological Transport, Cholesterol, Endocytosis, Homeostasis, Humans, Hyperlipoproteinemia Type II, Kinetics, Lipid Metabolism, Inborn Errors, Lipoproteins, HDL, Lipoproteins, LDL, Models, Biological, Mutation, Receptors, LDL
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