ArticleThe Biochemical journal1999
Functional and structural properties of lipid-associated apolipoprotein J (clusterin).
Article in The Biochemical journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- The Role of Clusterin Transporter in the Pathogenesis of Alzheimer's Disease at the Blood-Brain Barrier Interface: A Systematic Review.Biomolecules · 2022Pooled it
- Partially Replacing Dietary Carbohydrate With Unsaturated Fat or Protein Shifts Protein-Based HDL Subspecies Toward Lower Coronary Heart Disease Risk.Arteriosclerosis, thrombosis, and vascular biology · 2026Trial
- Receptor-mediated endocytosis by Megalin: Exploring its role in ligand interaction and disease mechanisms.Genes & diseases · 2026Review
- De-2-hydroxyisobutyrylation of clusterin modulates neuropathology and memory deficits in an Alzheimer's disease mouse model.Cell communication and signaling : CCS · 2026Article
- Structural analyses define the molecular basis of clusterin chaperone function.Nature structural & molecular biology · 2025Article
- Article
- The early diagnosis of Alzheimer's disease: Blood-based panel biomarker discovery by proteomics and metabolomics.CNS neuroscience & therapeutics · 2024Review
- The presence of circulating human apolipoprotein J reduces the occurrence of cerebral microbleeds in a transgenic mouse model with cerebral amyloid angiopathy.Alzheimer's research & therapy · 2024Article
- Alzheimer's genes in microglia: a risk worth investigating.Molecular neurodegeneration · 2023Review
- Clusterin/apolipoprotein J, its isoforms and Alzheimer's disease.Frontiers in aging neuroscience · 2023Article
- Clusterin Binding Modulates the Aggregation and Neurotoxicity of Amyloid-β(1-42).Molecular neurobiology · 2022Article
- Lipoproteins in the Central Nervous System: From Biology to Pathobiology.Annual review of biochemistry · 2022Review
- Exploring the Role of CLU in the Pathogenesis of Alzheimer's Disease.Neurotoxicity research · 2021Review
- Clusterin secreted from astrocyte promotes excitatory synaptic transmission and ameliorates Alzheimer's disease neuropathology.Molecular neurodegeneration · 2021Article
- Comparison of Plasma Lipoprotein Composition and Function in Cerebral Amyloid Angiopathy and Alzheimer's Disease.Biomedicines · 2021Article
- Kidney Diseases: The Age of Molecular Markers.Advances in experimental medicine and biology · 2021Article
- Extracellular HSP90 Machineries Build Tumor Microenvironment and Boost Cancer Progression.Frontiers in cell and developmental biology · 2021Review
- Article
- Sex differences in Alzheimer's disease: Understanding the molecular impact.Brain research · 2019Review
- Blood-Brain Barrier: From Physiology to Disease and Back.Physiological reviews · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Apolipoprotein J (apoJ, clusterin) is a multifunctional protein normally associated with lipids in plasma and cerebrospinal fluid, and secreted as lipoparticles by hepatocytes and astrocytes. To investigate whether the structural and functional properties of apoJ are modulated upon binding to lipids, we prepared apoJ high-density lipoprotein (HDL)-like particles employing either synthetic or plasma HDL-derived lipids. The majority of the resulting lipoparticles contained one molecule of apoJ per particle and exhibited the same alpha2 electrophoretic mobility characteristic of apoJ-containing plasma HDL. Particle size seemed to be dependent on the presence of cholesterol in the lipid mixture and ranged from diameters of 10 nm in the presence of cholesterol to 20 nm in the absence of cholesterol. CD analysis and Fourier-transform infrared spectroscopy revealed similar changes in the apoJ secondary structure induced by its incorporation into lipoparticles, namely a decrease in alpha-helix content and an increase in beta-turn structures. Two functional assays, the binding interaction with Alzheimer's amyloid beta peptides and the inhibitory activity of the complement membrane-attack complex, did not detect any changes in apoJ activity following its lipidation (P>0.05). On the contrary, the binding affinity to the cellular receptor megalin was enhanced significantly (P<0.01) after the association with lipids; the K(d) value decreased from 78.8+/-10.7 nM for the delipidated form to 37. 0+/-7.3 nM for apoJ-HDL. Although it is not known whether the structural changes observed are directly responsible for the higher receptor-binding affinity, the data suggest that the complement inhibition and amyloid beta-binding motifs are located in areas of the molecule different from those involved in the apoJ-megalin interaction.
Indexed as
Identifiers
10567218PMC1220653W2018957701What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.